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Induced Septic sentence examples within acute kidney injury

acute kidney injury

Background This study sought to compare the therapeutic effects of angiotensin II (ANG II) and norepinephrine (NE) on cecal ligation and puncture (CLP)-induced septic acute kidney injury (AKI) in rats.

Angiotensin II-mediated improvement of renal mitochondrial function via the AMPK/PGC-1α/NRF-2 pathway is superior to norepinephrine in a rat model of septic shock associated with acute renal injury.

acute kidney injury

BACKGROUND We intended to investigate the function of circular RNA RasGEF domain family member 1B (circ_RASGEF1B) in lipopolysaccharide (LPS)-induced septic acute kidney injury (AKI) cell model and its associated mechanism.

Circ_RASGEF1B Promotes LPS-Induced Apoptosis and Inflammatory Response by Targeting MicroRNA-146a-5p/Pdk1 Axis in Septic Acute Kidney Injury Cell Model.

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Induced Septic sentence examples within Lp Induced Septic

Lp Induced Septic

Conclusion: Significant improvement was noted in survival time, lesser tissue damage and better lung physiology by treating with Bronco T in LPS induced septicemia.

Bronco T (Shirisadi kasaya), a polyherbal formulation ameliorates LPS induced septicemia in rats

Lp Induced Septic

Conclusion miR-144−3 can promote LPS induced septic ALI through downregulating Caveolin-2 to activate the JAK/STAT signal pathway.

MicroRNA-144-3p enhances LPS induced septic acute lung injury in mice through downregulating Caveolin-2.

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Induced Septic sentence examples within induced septic shock

induced septic shock

In conclusion, FTO is involved in inflammatory response of LPS-induced septic shock and inhibition of FTO is promising for the treatment of septic shock.

Targeted Inhibition of FTO Demethylase Protects Mice Against LPS-Induced Septic Shock by Suppressing NLRP3 Inflammasome

induced septic shock

The expression of steroidogenic enzymes and corticosterone production was assessed RESULTS: Genetic deficiency of TREM2 caused significantly higher corticosterone levels at the early stage of LPS-induced septic shock; whereas TREM2 deficiency neither increased CRH and ACTH nor exacerbated the inflammation in adrenocortical tissue during septic shock.

Triggering receptor expressed on myeloid Cells-2 (TREM2) inhibits steroidogenesis in adrenocortical cell by macrophage-derived exosomes in lipopolysaccharide-induced septic shock

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Induced Septic sentence examples within induced septic mouse

induced septic mouse

In the cecal slurry (CS)-induced septic mouse model, we performed three different kinds of behavioral tests, open-field test, marble burying test, and forced swimming test, and observed anxiety-like behavior in septic mice.

Infiltrated regulatory T cells and Th2 cells in the brain contribute to attenuation of sepsis-associated encephalopathy and alleviation of mental impairments in mice with polymicrobial sepsis

induced septic mouse

The results showed that pretreatment with RMT (30 mg kg-1  d-1 , ip, for 3 days) significantly inhibited acute inflammatory responses in LPS-induced septic mice.

Rhodomeroterpene alleviates macrophage infiltration and the inflammatory response in renal tissue to improve acute kidney injury.

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Induced Septic sentence examples within induced septic rat

induced septic rat

Using the cecum ligation puncture (CLP) induced septic rat and LPS treated pulmonary vein endothelial cells(PVECs), the role of AQPs in the regulation of the permeability of pulmonary vascular, and its relationship to Ss-31 were studied.

The role of AQP3 in the vascular leakage of sepsis and the protective effect of Ss-31.

induced septic rat

These identified differential metabolites were majorly involved in arginine and proline metabolism, suggesting that XBJ injection is capable of improving metabolic disorders in CLP-induced septic rat to a certain extent.

Xuebijing Injection Affects the Dynamic Change of Metabolism in CLP-Induced Septic Rats

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Induced Septic sentence examples within induced septic cardiomyopathy

induced septic cardiomyopathy

Further study demonstrated that pharmacological inhibition of 5-Lox prevented CLP-induced septic cardiomyopathy (SCM).

Inhibition of 5-Lipoxygenase Is Associated with Downregulation of the Leukotriene B4 Receptor 1/ Interleukin-12p35 Pathway and Ameliorates Sepsis-Induced Myocardial Injury.

induced septic cardiomyopathy

HOTAIR levels were interfered by AAV9-sh-HOTAIR in LPS-induced septic cardiomyopathy mice.

LncRNA HOTAIR Promotes LPS-Induced Inflammation and Apoptosis of Cardiomyocytes via Lin28-Mediated PDCD4 Stability.

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Induced Septic sentence examples within induced septic arthritis

induced septic arthritis

aureus–induced septic arthritis still requires detailed investigation.

Selective Activation of MST1/2 Kinases by Retinoid Agonist Adapalene Abrogates AURKA-Regulated Septic Arthritis

induced septic arthritis

aureus induced septic arthritis in rabbits.

Efficacy evaluation of ethanolic extract of Tamarindus indica L. leaves as possible alternate therapy in septic arthritis model of rabbit

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Induced Septic sentence examples within induced septic ali

induced septic ali

The results of hematoxylin and eosin, respiratory function detection, malondialdehyde level and superoxide dismutase activity determination and ELSIA demonstrated that taurine significantly alleviated lung injury, restored respiratory function, reduced oxidation and decreased the concentrations of inflammatory factors in CLP-induced septic ALI model rats.

Protective effect of taurine on sepsis-induced lung injury via inhibiting the p38/MAPK signaling pathway

induced septic ali

Conclusion miR-144−3 can promote LPS induced septic ALI through downregulating Caveolin-2 to activate the JAK/STAT signal pathway.

MicroRNA-144-3p enhances LPS induced septic acute lung injury in mice through downregulating Caveolin-2.

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Induced Septic sentence examples within induced septic injury

induced septic injury

OBJECTIVE The aim of this study was to explore the role of alprostadil (Alp) in cecal ligation and puncture (CLP)-induced septic injury in rats and its possible mechanism of action.

Alprostadil alleviates liver injury in septic rats via TLR4/NF-κB pathway.

induced septic injury

Multispectral optoacoustic imaging showed that cecal ligation and puncture (CLP)-induced septic injury caused impaired renal excretion, which was improved in DHHC21 functional deficient (Zdhhc21dep/dep) mice.

DHHC21 Deficiency Attenuates Renal Dysfunction During Septic Injury

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Induced Septic sentence examples within induced septic aki

induced septic aki

We showed an activation of RIP3, accompanied by an accumulation of the autophagosome marker LC3II and the autophagic substrate p62, in the kidneys of lipopolysaccharide (LPS)-induced septic AKI mice and LPS-treated cultured renal proximal tubular epithelial cells (PTECs).

RIP3 impedes transcription factor EB to suppress autophagic degradation in septic acute kidney injury

induced septic aki

Furthermore, fisetin effectively reduced the number of TUNEL positive apoptotic cells and suppressed apoptotic protein of Bcl-2, BAX and cleaved caspase-3 in the kidneys of LPS-induced septic AKI.

Flavonoid fisetin alleviates kidney inflammation and apoptosis via inhibiting Src-mediated NF-κB p65 and MAPK signaling pathways in septic AKI mice.

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Induced Septic sentence examples within induced septic cardiac

induced septic cardiac

Although epoxyeicosatrienoic acids (EETs) have multiple protective effects against different diseases, whether they can improve the pathogenesis of lipopolysaccharide (LPS)-induced septic cardiac dysfunction remains unknown.

Epoxyeicosatrienoic Acids Prevent Cardiomyocytes against Sepsis by A2AR-induced Activation of PI3K and PPARγ.

induced septic cardiac

Furthermore, a total of 10 hub genes NDUFB5, TIMMDC1, VDAC3, COQ10A, MRPL16 (mitochondrial ribosomal protein L16), C3orf43, TMEM182, DLAT, NDUFA8, and PDHB (pyruvate dehydrogenase E1 beta subunit) in the blue module were identified at transcriptional level and further validated at translational level in myocardium of an lipopolysaccharide-induced septic cardiac dysfunction mouse model.

Potentially Critical Roles of NDUFB5, TIMMDC1, and VDAC3 in the Progression of Septic Cardiomyopathy Through Integrated Bioinformatics Analysis.

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Induced Septic sentence examples within induced septic model

induced septic model

Mice pretreated with NTS intraperitoneally displayed improved survival rate and extended survival time in LPS‐ and polymicrobe‐induced septic models, respectively.

Nitrosonisoldipine is a selective inhibitor of inflammatory caspases and protects against pyroptosis and related septic shock

induced septic model

In our previous work, we found cannabinoid receptor Ⅱ(CB2R) inhibited the expression of HMGB1 in lipopolysaccharide (LPS)-induced septic models in vivo and in vitro, but the underlying mechanism is still unclear.

Cannabinoid receptor 2 promotes the intracellular degradation of HMGB1 via the autophagy-lysosome pathway in macrophage.

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Induced Septic sentence examples within induced septic death

induced septic death

Importantly, the pharmacologic inhibition of the AGER-ALOX5 pathway or global depletion (Ager−/−) or conditional depletion of AGER in myeloid cells (AgerMye−/−) protects against lipopolysaccharide-induced septic death in poly(I:C)-primed mice.

AGER-Mediated Lipid Peroxidation Drives Caspase-11 Inflammasome Activation in Sepsis

induced septic death

Moreover, C-23, administered at a clinically well-tolerated dose, inhibits LPS-induced septic death and IL-1β secretion in mice.

Abstract A132: Identification of pyroptosis inhibitors that target a reactive cysteine in gasdermin D

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Induced Septic sentence examples within induced septic response

induced septic response

Our study illustrates an example of drug repositioning of Biapenem (BIPM), a carbapenem antibiotic, for the modulation of HMGB1-induced septic responses.

Biapenem reduces sepsis mortality via barrier protective pathways against HMGB1-mediated septic responses.

induced septic response

This suppression of TGFBIp-mediated and CLP-induced septic responses indicates that collismycin C is a potential therapeutic agent for various severe vascular inflammatory diseases, with inhibition of the TGFBIp signaling pathway as the mechanism of action.

Suppressive functions of collismycin C in TGFBIp-mediated septic responses

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Induced Septic sentence examples within induced septic lung

induced septic lung

Here, we investigated the protective efficacy of protocatechuic acid (PCA) against lipopolysaccharide (LPS)-induced septic lung injury.

Protocatechuic acid attenuates lipopolysaccharide-induced septic lung injury in mice: The possible role through suppressing oxidative stress, inflammation and apoptosis.

induced septic lung

We found that the GFP expression pattern in the Hdc-GFP mice faithfully recapitulated that of conventional histamine-producing cells and that the GFP expression level mirrored the increased Hdc expression in lipopolysaccharide (LPS)-induced septic lungs.

Lipopolysaccharide-induced expansion of histidine decarboxylase-expressing Ly6G+ myeloid cells identified by exploiting histidine decarboxylase BAC-GFP transgenic mice

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Induced Septic sentence examples within induced septic acute

induced septic acute

Background This study sought to compare the therapeutic effects of angiotensin II (ANG II) and norepinephrine (NE) on cecal ligation and puncture (CLP)-induced septic acute kidney injury (AKI) in rats.

Angiotensin II-mediated improvement of renal mitochondrial function via the AMPK/PGC-1α/NRF-2 pathway is superior to norepinephrine in a rat model of septic shock associated with acute renal injury.

induced septic acute

BACKGROUND We intended to investigate the function of circular RNA RasGEF domain family member 1B (circ_RASGEF1B) in lipopolysaccharide (LPS)-induced septic acute kidney injury (AKI) cell model and its associated mechanism.

Circ_RASGEF1B Promotes LPS-Induced Apoptosis and Inflammatory Response by Targeting MicroRNA-146a-5p/Pdk1 Axis in Septic Acute Kidney Injury Cell Model.

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More Induced Septic sentence examples
10.26355/eurrev_202102_24869

OBJECTIVE The aim of this study was to explore the role of alprostadil (Alp) in cecal ligation and puncture (CLP)-induced septic injury in rats and its possible mechanism of action.

Alprostadil alleviates liver injury in septic rats via TLR4/NF-κB pathway.

More Induced Septic sentence examples
10.1016/j.bbi.2020.11.010

In the cecal slurry (CS)-induced septic mouse model, we performed three different kinds of behavioral tests, open-field test, marble burying test, and forced swimming test, and observed anxiety-like behavior in septic mice.

Infiltrated regulatory T cells and Th2 cells in the brain contribute to attenuation of sepsis-associated encephalopathy and alleviation of mental impairments in mice with polymicrobial sepsis

More Induced Septic sentence examples
10.1096/fj.202100981RR

The results showed that pretreatment with RMT (30 mg kg-1  d-1 , ip, for 3 days) significantly inhibited acute inflammatory responses in LPS-induced septic mice.

Rhodomeroterpene alleviates macrophage infiltration and the inflammatory response in renal tissue to improve acute kidney injury.

More Induced Septic sentence examples
10.3389/fimmu.2021.663295

In conclusion, FTO is involved in inflammatory response of LPS-induced septic shock and inhibition of FTO is promising for the treatment of septic shock.

Targeted Inhibition of FTO Demethylase Protects Mice Against LPS-Induced Septic Shock by Suppressing NLRP3 Inflammasome

More Induced Septic sentence examples
10.1016/j.mce.2021.111178

The expression of steroidogenic enzymes and corticosterone production was assessed RESULTS: Genetic deficiency of TREM2 caused significantly higher corticosterone levels at the early stage of LPS-induced septic shock; whereas TREM2 deficiency neither increased CRH and ACTH nor exacerbated the inflammation in adrenocortical tissue during septic shock.

Triggering receptor expressed on myeloid Cells-2 (TREM2) inhibits steroidogenesis in adrenocortical cell by macrophage-derived exosomes in lipopolysaccharide-induced septic shock

More Induced Septic sentence examples
10.1016/j.freeradbiomed.2021.02.034

Further study demonstrated that pharmacological inhibition of 5-Lox prevented CLP-induced septic cardiomyopathy (SCM).

Inhibition of 5-Lipoxygenase Is Associated with Downregulation of the Leukotriene B4 Receptor 1/ Interleukin-12p35 Pathway and Ameliorates Sepsis-Induced Myocardial Injury.

More Induced Septic sentence examples
10.1002/eji.202048936

6, that strongly inhibited IFN‐γ production and LPS‐induced septic shock after viral infection, we demonstrate the critical role played by IL‐12 in the rejection of male skin graft by female C57BL/6 syngeneic recipients and in the clearance of an immunogenic mastocytoma tumor variant by DBA/2 mice, but not in a parent to F1 immune aggression model nor in MOG‐induced EAE, which was clearly prevented by anti‐p40 mAb C17.

Novel antibodies that selectively block mouse IL‐12 enable the re‐evaluation of the role of IL‐12 in immune protection and pathology

More Induced Septic sentence examples
10.1093/intimm/dxab029

We generated mice with USP18 or/and TAK1 deficiency in macrophages (USP18 MKO mice, TAK1 MKO mice and USP18 MKO TAK1 MKO mice) and established lipopolysaccharides (LPS)-induced septic mice model.

USP18 negatively regulates and inhibits lipopolysaccharides-induced sepsis by targeting TAK1 activity.

More Induced Septic sentence examples
10.1155/2021/8889313

In addition, administration of recombinant sRAGE protein suppressed the activation of the RAGE/NF-κB signaling pathway and ameliorated pulmonary oxidative stress, inflammation, and lung injury in CLP-induced septic mice.

Upregulation of Matrix Metalloproteinase-9 Protects against Sepsis-Induced Acute Lung Injury via Promoting the Release of Soluble Receptor for Advanced Glycation End Products

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10.1038/s41419-021-03508-y

Moreover, two SIRT1 activators, resveratrol and polydatin, attenuated SAKI in CLP-induced septic mice.

SIRT1 attenuates sepsis-induced acute kidney injury via Beclin1 deacetylation-mediated autophagy activation

More Induced Septic sentence examples
10.1007/s43440-020-00212-0

Our study illustrates an example of drug repositioning of Biapenem (BIPM), a carbapenem antibiotic, for the modulation of HMGB1-induced septic responses.

Biapenem reduces sepsis mortality via barrier protective pathways against HMGB1-mediated septic responses.

More Induced Septic sentence examples
10.3389/fimmu.2021.620238

However, the specific mechanism of Pin1 regulation in LPS-induced septic shock is unclear.

Pin1 Promotes NLRP3 Inflammasome Activation by Phosphorylation of p38 MAPK Pathway in Septic Shock

More Induced Septic sentence examples
10.1097/FJC.0000000000001050

Using the cecum ligation puncture (CLP) induced septic rat and LPS treated pulmonary vein endothelial cells(PVECs), the role of AQPs in the regulation of the permeability of pulmonary vascular, and its relationship to Ss-31 were studied.

The role of AQP3 in the vascular leakage of sepsis and the protective effect of Ss-31.

More Induced Septic sentence examples
10.1007/s10753-021-01431-0

HOTAIR levels were interfered by AAV9-sh-HOTAIR in LPS-induced septic cardiomyopathy mice.

LncRNA HOTAIR Promotes LPS-Induced Inflammation and Apoptosis of Cardiomyocytes via Lin28-Mediated PDCD4 Stability.

More Induced Septic sentence examples
10.1111/jfbc.13915

Here, we investigated the protective efficacy of protocatechuic acid (PCA) against lipopolysaccharide (LPS)-induced septic lung injury.

Protocatechuic acid attenuates lipopolysaccharide-induced septic lung injury in mice: The possible role through suppressing oxidative stress, inflammation and apoptosis.

More Induced Septic sentence examples
10.4049/jimmunol.2001360

aureus–induced septic arthritis still requires detailed investigation.

Selective Activation of MST1/2 Kinases by Retinoid Agonist Adapalene Abrogates AURKA-Regulated Septic Arthritis

More Induced Septic sentence examples
10.21203/RS.3.RS-526582/V1

These identified differential metabolites were majorly involved in arginine and proline metabolism, suggesting that XBJ injection is capable of improving metabolic disorders in CLP-induced septic rat to a certain extent.

Xuebijing Injection Affects the Dynamic Change of Metabolism in CLP-Induced Septic Rats

More Induced Septic sentence examples
10.1002/ptr.7191

The results showed that emodin alleviated cardiac dysfunction, myocardial injury and improved survival rate in LPS‐induced septic mice.

Emodin alleviates LPS‐induced myocardial injury through inhibition of NLRP3 inflammasome activation

More Induced Septic sentence examples
10.1186/s10020-021-00323-1

Next, plasma desHMGB1 levels were examined in a cecal ligation and puncture (CLP)-induced septic mouse model treated with rTM.

Specific detection of high mobility group box 1 degradation product with a novel ELISA

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10.3892/mmr.2021.12292

The results of hematoxylin and eosin, respiratory function detection, malondialdehyde level and superoxide dismutase activity determination and ELSIA demonstrated that taurine significantly alleviated lung injury, restored respiratory function, reduced oxidation and decreased the concentrations of inflammatory factors in CLP-induced septic ALI model rats.

Protective effect of taurine on sepsis-induced lung injury via inhibiting the p38/MAPK signaling pathway

More Induced Septic sentence examples
10.21203/RS.3.RS-253174/V1

Multispectral optoacoustic imaging showed that cecal ligation and puncture (CLP)-induced septic injury caused impaired renal excretion, which was improved in DHHC21 functional deficient (Zdhhc21dep/dep) mice.

DHHC21 Deficiency Attenuates Renal Dysfunction During Septic Injury

More Induced Septic sentence examples
10.1016/j.intimp.2021.108106

GGPPS1 was upregulated in the lung tissues of CLP-induced septic mice.

Geranylgeranyl diphosphate synthase 1 knockdown suppresses NLRP3 inflammasome activity via promoting autophagy in sepsis-induced acute lung injury.

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10.1182/bloodadvances.2020002782

It also improved immunity during Escherichia coli-induced septic peritonitis.

The GPCR adaptor protein norbin suppresses the neutrophil-mediated immunity of mice to pneumococcal infection.

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10.1016/j.bmcl.2021.128106

Furthermore, its good performance of anti-inflammatory effect on LPS-induced multiple inflammatory cytokines production, carrageenan-induced paw edema, and endotoxin-induced septic mice, was observed.

Discovery of a novel inhibitor of nitric oxide production with potential therapeutic effect on acute inflammation.

More Induced Septic sentence examples
10.1038/s41419-021-03865-8

We showed an activation of RIP3, accompanied by an accumulation of the autophagosome marker LC3II and the autophagic substrate p62, in the kidneys of lipopolysaccharide (LPS)-induced septic AKI mice and LPS-treated cultured renal proximal tubular epithelial cells (PTECs).

RIP3 impedes transcription factor EB to suppress autophagic degradation in septic acute kidney injury

More Induced Septic sentence examples
10.1038/s41418-021-00803-1

Consequently, Trim26 deficiency protects mice from LPS-induced septic shock in vivo.

TRIM26 positively regulates the inflammatory immune response through K11-linked ubiquitination of TAB1.

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10.1126/scisignal.abe0387

Mice lacking NDPK-D were protected from LPS-induced septic shock.

A genome-wide screen uncovers multiple roles for mitochondrial nucleoside diphosphate kinase D in inflammasome activation

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10.1073/pnas.2015416118

The deficiency of ASB1 leads to less severe colitis and intestinal inflammation and protects mice from bacteria or lipopolysaccharide-induced septic shock.

An unconventional role of an ASB family protein in NF-κB activation and inflammatory response during microbial infection and colitis

More Induced Septic sentence examples
10.1002/eji.202048937

Mice pretreated with NTS intraperitoneally displayed improved survival rate and extended survival time in LPS‐ and polymicrobe‐induced septic models, respectively.

Nitrosonisoldipine is a selective inhibitor of inflammatory caspases and protects against pyroptosis and related septic shock

More Induced Septic sentence examples
10.3389/fimmu.2021.653344

We also explored the downstream cytokines released by neutrophils following miR-let-7b treatment and its therapeutic effects in cecal ligation and puncture (CLP)-induced septic mice.

MicroLet-7b Regulates Neutrophil Function and Dampens Neutrophilic Inflammation by Suppressing the Canonical TLR4/NF-κB Pathway

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10.1038/s41598-021-89983-x

Multispectral optoacoustic imaging showed that cecal ligation and puncture (CLP)-induced septic injury caused impaired renal excretion, which was improved in DHHC21 functional deficient (Zdhhc21dep/dep) mice.

DHHC21 deficiency attenuates renal dysfunction during septic injury

More Induced Septic sentence examples
10.2147/JIR.S305202

Results Our results showed that the diet riches in methyl donors exacerbated mortality, organ injury, and circulating levels of inflammatory mediators in CLP-induced septic mice model, compared to the control diet group.

Methyl Diet Enhanced Sepsis-Induced Mortality Through Altering Gut Microbiota

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10.1016/j.jep.2021.113783

AIM OF THE STUDY To investigate the protective effect of RDN on both lipopolysaccharides (LPS)- and cecal ligation and puncture (CLP)-induced septic mice.

Reduning injection and its effective constituent luteoloside protect against sepsis partly via inhibition of HMGB1/TLR4/NF-κB/MAPKs signaling pathways.

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10.1515/med-2021-0008

In this research, we attempted to explain the effect and the related molecular mechanisms of ABIN1 in lipopolysaccharide (LPS)-induced septic mice or RAW264.

Expression and role of ABIN1 in sepsis: In vitro and in vivo studies

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10.1007/s10753-021-01436-9

In this study, NEAT1 and POU domain class 2 transcription factor 1 (POU2F1) were highly expressed in LPS-induced septic RAW264.

LncRNA NEAT1 Promotes Inflammatory Response in Sepsis via the miR-31-5p/POU2F1 Axis

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10.1016/j.prostaglandins.2021.106595

Although epoxyeicosatrienoic acids (EETs) have multiple protective effects against different diseases, whether they can improve the pathogenesis of lipopolysaccharide (LPS)-induced septic cardiac dysfunction remains unknown.

Epoxyeicosatrienoic Acids Prevent Cardiomyocytes against Sepsis by A2AR-induced Activation of PI3K and PPARγ.

More Induced Septic sentence examples
10.1016/j.intimp.2021.107639

The cecal ligation and puncture-induced septicemia mice and the LPS-stimulated H9C2 cardiomyocytes were prepared as the models in vivo and in vitro, separately.

Piceatannol protects against sepsis-induced myocardial dysfunction via direct inhibition of JAK2.

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10.3389/fphar.2021.648688

However, the beneficial effects of LIQ in lipopolysaccharides (LPS)-induced septic cardiomyopathy (SCM) has not been reported.

Liquiritin Attenuates Lipopolysaccharides-Induced Cardiomyocyte Injury via an AMP-Activated Protein Kinase-Dependent Signaling Pathway

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10.1007/s10787-021-00797-9

A recent article by Maayah and coworkers elegantly described a survival benefit with the use of the SGLT2 inhibitor Empagliflozin (Empa) in a murine model of LPSinduced septic shock (Maayah et al.

Anti-inflammatory potential of Empagliflozin

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10.1155/2021/5535562

This study is aimed at evaluating the effects of βS on the biomarkers of inflammation and liver function in cecal ligation and puncture- (CLP-) induced septic rats.

β-Sitosterol Alters the Inflammatory Response in CLP Rat Model of Sepsis by Modulation of NFκB Signaling

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10.1007/s13596-021-00595-2

Systemic anaphylaxis was studied using compound 48/80 systemic anaphylaxis and lipopolysaccharide (LPS)-induced septic shock models.

Cutaneous and systemic anti-allergic potential of xylopic acid in rodents

Keywords related to Induced

Induced Septic
Encyclopedia

What is/are Induced Septic?

Induced Septic - OBJECTIVE The aim of this study was to explore the role of alprostadil (Alp) in cecal ligation and puncture (CLP)-induced septic injury in rats and its possible mechanism of action. [1] In the cecal slurry (CS)-induced septic mouse model, we performed three different kinds of behavioral tests, open-field test, marble burying test, and forced swimming test, and observed anxiety-like behavior in septic mice. [2] The results showed that pretreatment with RMT (30 mg kg-1  d-1 , ip, for 3 days) significantly inhibited acute inflammatory responses in LPS-induced septic mice. [3] In conclusion, FTO is involved in inflammatory response of LPS-induced septic shock and inhibition of FTO is promising for the treatment of septic shock. [4] The expression of steroidogenic enzymes and corticosterone production was assessed RESULTS: Genetic deficiency of TREM2 caused significantly higher corticosterone levels at the early stage of LPS-induced septic shock; whereas TREM2 deficiency neither increased CRH and ACTH nor exacerbated the inflammation in adrenocortical tissue during septic shock. [5] Further study demonstrated that pharmacological inhibition of 5-Lox prevented CLP-induced septic cardiomyopathy (SCM). [6] 6, that strongly inhibited IFN‐γ production and LPS‐induced septic shock after viral infection, we demonstrate the critical role played by IL‐12 in the rejection of male skin graft by female C57BL/6 syngeneic recipients and in the clearance of an immunogenic mastocytoma tumor variant by DBA/2 mice, but not in a parent to F1 immune aggression model nor in MOG‐induced EAE, which was clearly prevented by anti‐p40 mAb C17. [7] We generated mice with USP18 or/and TAK1 deficiency in macrophages (USP18 MKO mice, TAK1 MKO mice and USP18 MKO TAK1 MKO mice) and established lipopolysaccharides (LPS)-induced septic mice model. [8] In addition, administration of recombinant sRAGE protein suppressed the activation of the RAGE/NF-κB signaling pathway and ameliorated pulmonary oxidative stress, inflammation, and lung injury in CLP-induced septic mice. [9] Moreover, two SIRT1 activators, resveratrol and polydatin, attenuated SAKI in CLP-induced septic mice. [10] Our study illustrates an example of drug repositioning of Biapenem (BIPM), a carbapenem antibiotic, for the modulation of HMGB1-induced septic responses. [11] However, the specific mechanism of Pin1 regulation in LPS-induced septic shock is unclear. [12] Using the cecum ligation puncture (CLP) induced septic rat and LPS treated pulmonary vein endothelial cells(PVECs), the role of AQPs in the regulation of the permeability of pulmonary vascular, and its relationship to Ss-31 were studied. [13] HOTAIR levels were interfered by AAV9-sh-HOTAIR in LPS-induced septic cardiomyopathy mice. [14] Here, we investigated the protective efficacy of protocatechuic acid (PCA) against lipopolysaccharide (LPS)-induced septic lung injury. [15] aureus–induced septic arthritis still requires detailed investigation. [16] These identified differential metabolites were majorly involved in arginine and proline metabolism, suggesting that XBJ injection is capable of improving metabolic disorders in CLP-induced septic rat to a certain extent. [17] The results showed that emodin alleviated cardiac dysfunction, myocardial injury and improved survival rate in LPS‐induced septic mice. [18] Next, plasma desHMGB1 levels were examined in a cecal ligation and puncture (CLP)-induced septic mouse model treated with rTM. [19] The results of hematoxylin and eosin, respiratory function detection, malondialdehyde level and superoxide dismutase activity determination and ELSIA demonstrated that taurine significantly alleviated lung injury, restored respiratory function, reduced oxidation and decreased the concentrations of inflammatory factors in CLP-induced septic ALI model rats. [20] Multispectral optoacoustic imaging showed that cecal ligation and puncture (CLP)-induced septic injury caused impaired renal excretion, which was improved in DHHC21 functional deficient (Zdhhc21dep/dep) mice. [21] GGPPS1 was upregulated in the lung tissues of CLP-induced septic mice. [22] It also improved immunity during Escherichia coli-induced septic peritonitis. [23] Furthermore, its good performance of anti-inflammatory effect on LPS-induced multiple inflammatory cytokines production, carrageenan-induced paw edema, and endotoxin-induced septic mice, was observed. [24] We showed an activation of RIP3, accompanied by an accumulation of the autophagosome marker LC3II and the autophagic substrate p62, in the kidneys of lipopolysaccharide (LPS)-induced septic AKI mice and LPS-treated cultured renal proximal tubular epithelial cells (PTECs). [25] Consequently, Trim26 deficiency protects mice from LPS-induced septic shock in vivo. [26] Mice lacking NDPK-D were protected from LPS-induced septic shock. [27] The deficiency of ASB1 leads to less severe colitis and intestinal inflammation and protects mice from bacteria or lipopolysaccharide-induced septic shock. [28] Mice pretreated with NTS intraperitoneally displayed improved survival rate and extended survival time in LPS‐ and polymicrobe‐induced septic models, respectively. [29] We also explored the downstream cytokines released by neutrophils following miR-let-7b treatment and its therapeutic effects in cecal ligation and puncture (CLP)-induced septic mice. [30] Multispectral optoacoustic imaging showed that cecal ligation and puncture (CLP)-induced septic injury caused impaired renal excretion, which was improved in DHHC21 functional deficient (Zdhhc21dep/dep) mice. [31] Results Our results showed that the diet riches in methyl donors exacerbated mortality, organ injury, and circulating levels of inflammatory mediators in CLP-induced septic mice model, compared to the control diet group. [32] AIM OF THE STUDY To investigate the protective effect of RDN on both lipopolysaccharides (LPS)- and cecal ligation and puncture (CLP)-induced septic mice. [33] In this research, we attempted to explain the effect and the related molecular mechanisms of ABIN1 in lipopolysaccharide (LPS)-induced septic mice or RAW264. [34] In this study, NEAT1 and POU domain class 2 transcription factor 1 (POU2F1) were highly expressed in LPS-induced septic RAW264. [35] Although epoxyeicosatrienoic acids (EETs) have multiple protective effects against different diseases, whether they can improve the pathogenesis of lipopolysaccharide (LPS)-induced septic cardiac dysfunction remains unknown. [36] The cecal ligation and puncture-induced septicemia mice and the LPS-stimulated H9C2 cardiomyocytes were prepared as the models in vivo and in vitro, separately. [37] However, the beneficial effects of LIQ in lipopolysaccharides (LPS)-induced septic cardiomyopathy (SCM) has not been reported. [38] A recent article by Maayah and coworkers elegantly described a survival benefit with the use of the SGLT2 inhibitor Empagliflozin (Empa) in a murine model of LPSinduced septic shock (Maayah et al. [39] This study is aimed at evaluating the effects of βS on the biomarkers of inflammation and liver function in cecal ligation and puncture- (CLP-) induced septic rats. [40] Systemic anaphylaxis was studied using compound 48/80 systemic anaphylaxis and lipopolysaccharide (LPS)-induced septic shock models. [41]

acute kidney injury

Background This study sought to compare the therapeutic effects of angiotensin II (ANG II) and norepinephrine (NE) on cecal ligation and puncture (CLP)-induced septic acute kidney injury (AKI) in rats. [1] BACKGROUND We intended to investigate the function of circular RNA RasGEF domain family member 1B (circ_RASGEF1B) in lipopolysaccharide (LPS)-induced septic acute kidney injury (AKI) cell model and its associated mechanism. [2] Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection The lung failure for sepsis is reported in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused Coronavirus Disease 2019 (COVID-19), and patients in the intensive care unit (ICU) We previously reported that anisodamine hydrobromide (Ani HBr), an extract from the Chinese herb Anisodus tanguticus (Maxim) Pascher, could alleviate acute kidney injury in septic rats In this study, we test whether Ani HBr protects against lung injury in septic rats Adult specific pathogen-free (SPF) male Sprague-Dawley (SD) rats were intraperitoneally injected with 5 mg/kg lipopolysaccharide (LPS) for 4 h or underwent cecal ligation and puncture (CLP) surgery for 24 h, followed by another 24 h treatment of Ani HBr (0, 1 8 and 5 4 mg/kg) or atropine (5 mg/kg) via tail intravenous injection Lung injury was evaluated by hematoxylin and eosin (H&E) staining, serum levels of creatine kinase (CK), lactic acid (LA), lactic dehydrogenase (LDH), CXCL8 and tumor necrosis factor (TNF-α), serum and lung tissue levels of superoxide dismutase (SOD) and malonaldehyde (MDA), immunohistochemistry (IHC) staining of GSDMD and NLRP3, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay The protective mechanisms of Ani HBr against apoptosis and pyroptosis in lung tissues were examined by detecting the IL-1?, (pro) caspase-1, GSDMD and NLRP3 for pyroptosis, and (pro)caspase-3, Bcl-2 and Bax for apoptosis by Western Blot, respectively Results showed that Ani HBr alleviated histopathologic injuries of the lung including inflammatory cell infiltration, and alveolar damages and edema in LPS- and CLP-induced septic rats Ani HBr suppressed LPS- and CLP-induced CK, LA, LDH, CXCL8 and TNF-α in serum Ani HBr reduced MDA in serum and lung tissue in septic rats, while elevated SOD activity Ani HBr inhibited the positive cell rate of GSDMD and NLRP3 in lung sections induced by LPS and CLP, and inhibited the GSDMD and NLRP3 expression induced by LPS and CLP Ani HBr inhibited LPS- and CLP-induced apoptosis in lung tissues In accordance with the IHC staining results, Ani HBr inhibited expressions of IL-1?, NLRP 3, caspase-1 and GSDMD The proapoptotic markers including Bax and (pro) caspase 3 were reduced by Ani HBr, and antiapoptotic marker Bcl-2 was increased by Ani HBr The protective effects of Ani HBr at 5 4 mg/kg were better than 1 8 mg/kg and atropine Therefore, Ani HBr alleviates acute lung injury in septic rats, which provides evidence supporting the clinical therapy of lung injury by Ani HBr. [3]

Lp Induced Septic

Conclusion: Significant improvement was noted in survival time, lesser tissue damage and better lung physiology by treating with Bronco T in LPS induced septicemia. [1] Conclusion miR-144−3 can promote LPS induced septic ALI through downregulating Caveolin-2 to activate the JAK/STAT signal pathway. [2] By administrating the brusatol, the inhibition of Nrf2 enhanced the expression of NF-κB, inhibits the antioxidant responses, and further reverse the protective effect of LBP on the LPS induced septic kidney injury. [3]

induced septic shock

In conclusion, FTO is involved in inflammatory response of LPS-induced septic shock and inhibition of FTO is promising for the treatment of septic shock. [1] The expression of steroidogenic enzymes and corticosterone production was assessed RESULTS: Genetic deficiency of TREM2 caused significantly higher corticosterone levels at the early stage of LPS-induced septic shock; whereas TREM2 deficiency neither increased CRH and ACTH nor exacerbated the inflammation in adrenocortical tissue during septic shock. [2] 6, that strongly inhibited IFN‐γ production and LPS‐induced septic shock after viral infection, we demonstrate the critical role played by IL‐12 in the rejection of male skin graft by female C57BL/6 syngeneic recipients and in the clearance of an immunogenic mastocytoma tumor variant by DBA/2 mice, but not in a parent to F1 immune aggression model nor in MOG‐induced EAE, which was clearly prevented by anti‐p40 mAb C17. [3] However, the specific mechanism of Pin1 regulation in LPS-induced septic shock is unclear. [4] Consequently, Trim26 deficiency protects mice from LPS-induced septic shock in vivo. [5] Mice lacking NDPK-D were protected from LPS-induced septic shock. [6] The deficiency of ASB1 leads to less severe colitis and intestinal inflammation and protects mice from bacteria or lipopolysaccharide-induced septic shock. [7] A recent article by Maayah and coworkers elegantly described a survival benefit with the use of the SGLT2 inhibitor Empagliflozin (Empa) in a murine model of LPSinduced septic shock (Maayah et al. [8] Systemic anaphylaxis was studied using compound 48/80 systemic anaphylaxis and lipopolysaccharide (LPS)-induced septic shock models. [9] Here, we report that myeloid-deficient Becn1 (Becn1ΔM) mice develop neutrophilia and hypersusceptible to LPS-induced septic shock, with a high risk of developing spontaneous precursor (pre)-B cell lymphoma with elevated expressions of immunosuppressive molecules PD-L1 and IL-10. [10] In coincided with the in vitro results, ELL increased the survival and antagonized the hypothermia in the mice with LPS-induced septic shock. [11] Given its central immune-regulatory roles during tissue injury and LPS-induced septic shock, interventions aimed at HMGB1 signaling have been advocated as therapeutic options for various disease conditions. [12] Mice lacking Prdx4 show an increased susceptibility to LPS‐induced septic shock. [13] However, the mechanism of miR-21 in LPS-induced septic shock is still unclear. [14] In addition, the notion of monoclonal antibody as the magic bullet for endotoxin-induced septic shock is undergoing reexamination. [15] a choline kinase inhibitor attenuated inflammation in two acute experimental models of iL-1β-dependent inflammation (lipopolysaccharide-induced septic shock and air-pouch gouty arthritis). [16] A non-neutralizing anti-adrenomedullin antibody, Adrecizumab, may improve haemodynamic dysfunction during caecal ligation and puncture-induced septic shock in a murine model. [17] The in vivo effect of ELA was evaluated on LPS-induced septic shock in mice model. [18] Here, inhibition of fatty acid synthase by C75 improved neutrophil chemotaxis and increased the survival of mice with sepsis in cecal ligation puncture and lipopolysaccharide-induced septic shock models. [19] Importantly, Hrd1 deficiency in macrophages protects mice against lipopolysaccharide-induced septic shock, and knockdown of Usp15 in Hrd1-knockout macrophages restores the reduced IL-6 production. [20] AIM OF THE STUDY To investigate the effect of Shenfu injection on lipopolysaccharide (LPS)-induced septic shock in rabbits. [21] FXll KO mice are protected in LPS-induced septic shock and EAE models. [22] Rg6 was found to negatively regulate pro-inflammatory responses and severity in vivo, and thus induced recovery in mice with lipopolysaccharide (LPS)-induced septic shock and cecal ligation and puncture (CLP)-induced sepsis. [23] RESULTS Pirenzepine and atropine pretreatment improved survival rate of LPS-induced septic shock; in contrast, AF-DX116 accelerated death from sepsis. [24] RESULTS Pirenzepine and atropine pretreatment improved survival rate of LPS-induced septic shock; in contrast, AF-DX116 accelerated death from sepsis. [25] We present a case of metformin-associated lactic acidosis incited by pyelonephritis-induced septic shock where use of continuous renal replacement therapy (CRRT) led to good recovery. [26] Moreover, we investigated the antiseptic effect of Ps-K18 using a lipopolysaccharide or Escherichia coli K1-induced septic shock mouse model. [27]

induced septic mouse

In the cecal slurry (CS)-induced septic mouse model, we performed three different kinds of behavioral tests, open-field test, marble burying test, and forced swimming test, and observed anxiety-like behavior in septic mice. [1] The results showed that pretreatment with RMT (30 mg kg-1  d-1 , ip, for 3 days) significantly inhibited acute inflammatory responses in LPS-induced septic mice. [2] We generated mice with USP18 or/and TAK1 deficiency in macrophages (USP18 MKO mice, TAK1 MKO mice and USP18 MKO TAK1 MKO mice) and established lipopolysaccharides (LPS)-induced septic mice model. [3] In addition, administration of recombinant sRAGE protein suppressed the activation of the RAGE/NF-κB signaling pathway and ameliorated pulmonary oxidative stress, inflammation, and lung injury in CLP-induced septic mice. [4] Moreover, two SIRT1 activators, resveratrol and polydatin, attenuated SAKI in CLP-induced septic mice. [5] The results showed that emodin alleviated cardiac dysfunction, myocardial injury and improved survival rate in LPS‐induced septic mice. [6] Next, plasma desHMGB1 levels were examined in a cecal ligation and puncture (CLP)-induced septic mouse model treated with rTM. [7] GGPPS1 was upregulated in the lung tissues of CLP-induced septic mice. [8] Furthermore, its good performance of anti-inflammatory effect on LPS-induced multiple inflammatory cytokines production, carrageenan-induced paw edema, and endotoxin-induced septic mice, was observed. [9] We also explored the downstream cytokines released by neutrophils following miR-let-7b treatment and its therapeutic effects in cecal ligation and puncture (CLP)-induced septic mice. [10] Results Our results showed that the diet riches in methyl donors exacerbated mortality, organ injury, and circulating levels of inflammatory mediators in CLP-induced septic mice model, compared to the control diet group. [11] AIM OF THE STUDY To investigate the protective effect of RDN on both lipopolysaccharides (LPS)- and cecal ligation and puncture (CLP)-induced septic mice. [12] In this research, we attempted to explain the effect and the related molecular mechanisms of ABIN1 in lipopolysaccharide (LPS)-induced septic mice or RAW264. [13] In this study, we sought to explore the impact of MaR1 on metabolic dysfunction in cecal ligation and puncture- (CLP-) induced septic mice. [14] Additionally, in a lipopolysaccharide-induced septic mouse model, mice administered the probiotic 19 was highly resistant to Lps and exhibited decreased expression of inflammatory factors compared to Lps-treated control mice. [15] Collectively, our results provide a possible novel signaling axis involving MCPIP1/miR‐9/SIRT1 in LPS‐induced septic mice. [16] FMT decreased the percentage of G-MDSCs and monocytic MDSCs (M-MDSCs) in the spleens of LPS-induced septic mice. [17] In this study, we found that glycolytic inhibitor 2-deoxyglucose (2-DG) significantly improved the survival rate in cecal ligation and puncture (CLP)-induced septic mice. [18] In LPS-induced septic mice, FC-99 pretreated mice displayed lower expression of M1 markers together with the increased M2 marker CD206 and improvement of liver injury. [19] In this study we examined the effects of Tanshinone II-A (TSN), a widely used traditional Chinese medicine, on immunosuppression in experimental peritonitis induced septic mice. [20] Significance and Impact of Study: This study demonstrated the protective effects and mechanisms involved in the protective role of live combined Bacillus subtilis and Enterococcus faecium (LCBE) in CLP-induced septic mice model. [21] In this study, kinetic changes in the immune system were analyzed for 72 h in cecal ligation and puncture (CLP)-induced septic mice while preventing animal death by keeping body temperature. [22] Here, a caspase-1 inhibitor VX765 was treated with CLP-induced septic mice. [23] Consequently, we hypothesized that rTM reduces NET formation in the organs of LPS-induced septic mice. [24]

induced septic rat

Using the cecum ligation puncture (CLP) induced septic rat and LPS treated pulmonary vein endothelial cells(PVECs), the role of AQPs in the regulation of the permeability of pulmonary vascular, and its relationship to Ss-31 were studied. [1] These identified differential metabolites were majorly involved in arginine and proline metabolism, suggesting that XBJ injection is capable of improving metabolic disorders in CLP-induced septic rat to a certain extent. [2] Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection The lung failure for sepsis is reported in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused Coronavirus Disease 2019 (COVID-19), and patients in the intensive care unit (ICU) We previously reported that anisodamine hydrobromide (Ani HBr), an extract from the Chinese herb Anisodus tanguticus (Maxim) Pascher, could alleviate acute kidney injury in septic rats In this study, we test whether Ani HBr protects against lung injury in septic rats Adult specific pathogen-free (SPF) male Sprague-Dawley (SD) rats were intraperitoneally injected with 5 mg/kg lipopolysaccharide (LPS) for 4 h or underwent cecal ligation and puncture (CLP) surgery for 24 h, followed by another 24 h treatment of Ani HBr (0, 1 8 and 5 4 mg/kg) or atropine (5 mg/kg) via tail intravenous injection Lung injury was evaluated by hematoxylin and eosin (H&E) staining, serum levels of creatine kinase (CK), lactic acid (LA), lactic dehydrogenase (LDH), CXCL8 and tumor necrosis factor (TNF-α), serum and lung tissue levels of superoxide dismutase (SOD) and malonaldehyde (MDA), immunohistochemistry (IHC) staining of GSDMD and NLRP3, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay The protective mechanisms of Ani HBr against apoptosis and pyroptosis in lung tissues were examined by detecting the IL-1?, (pro) caspase-1, GSDMD and NLRP3 for pyroptosis, and (pro)caspase-3, Bcl-2 and Bax for apoptosis by Western Blot, respectively Results showed that Ani HBr alleviated histopathologic injuries of the lung including inflammatory cell infiltration, and alveolar damages and edema in LPS- and CLP-induced septic rats Ani HBr suppressed LPS- and CLP-induced CK, LA, LDH, CXCL8 and TNF-α in serum Ani HBr reduced MDA in serum and lung tissue in septic rats, while elevated SOD activity Ani HBr inhibited the positive cell rate of GSDMD and NLRP3 in lung sections induced by LPS and CLP, and inhibited the GSDMD and NLRP3 expression induced by LPS and CLP Ani HBr inhibited LPS- and CLP-induced apoptosis in lung tissues In accordance with the IHC staining results, Ani HBr inhibited expressions of IL-1?, NLRP 3, caspase-1 and GSDMD The proapoptotic markers including Bax and (pro) caspase 3 were reduced by Ani HBr, and antiapoptotic marker Bcl-2 was increased by Ani HBr The protective effects of Ani HBr at 5 4 mg/kg were better than 1 8 mg/kg and atropine Therefore, Ani HBr alleviates acute lung injury in septic rats, which provides evidence supporting the clinical therapy of lung injury by Ani HBr. [3] We used cecal ligation and puncture induced septic rats and lipopolysaccharide stimulated vascular endothelial cells (VECs) to establish models in vivo and in vitro, then the protective effects of Dex on the vascular endothelial barrier function of sepsis were observed, meanwhile, related mechanisms on regulating mitochondrial fission were further studied. [4] This study is aimed at evaluating the effects of βS on the biomarkers of inflammation and liver function in cecal ligation and puncture- (CLP-) induced septic rats. [5] The purpose of this set of data was to evaluate NF-κB gene expression in cecal ligation and puncture (CLP)- induced septic rats and associated hepatic cell changes. [6] More importantly, ADMSCs could improve the survival rate of CLP-induced septic rats. [7] The present study was designed to investigate the effects of rhubarb on the expression of GR and cellular immunity in burn-induced septic rats. [8] ALA treatment improved the survival rate, restored the loss of body weight and pro-inflammatory cytokines production in the serum of CLP-induced septic rats. [9] METHODS The oxidative stress parameters, antioxidant parameters and cytokine levels with or without lycopene treatment in LPS‑induced septic rats as well as in controls were measured in serum and tissue. [10] ConclusionsThese findings demonstrate that LDK378 treatment can improve microcirculation and reduce organ injuries in CLP-induced septic rats via the regulation of inflammatory cytokine secretion and the downstream signaling components of the ALK-STING pathway. [11]

induced septic cardiomyopathy

Further study demonstrated that pharmacological inhibition of 5-Lox prevented CLP-induced septic cardiomyopathy (SCM). [1] HOTAIR levels were interfered by AAV9-sh-HOTAIR in LPS-induced septic cardiomyopathy mice. [2] However, the beneficial effects of LIQ in lipopolysaccharides (LPS)-induced septic cardiomyopathy (SCM) has not been reported. [3] The aim of our study was to explore the in vivo and in vitro effects of irisin using an LPS-induced septic cardiomyopathy model. [4] Mitochondrial stress has been acknowledged as the pathogenesis for tumor necrosis factor‐α (TNF‐α)‐induced septic cardiomyopathy. [5] In the present study, Mst1 knockout mice were used in a lipopolysaccharide (LPS)‐induced septic cardiomyopathy model. [6]

induced septic arthritis

aureus–induced septic arthritis still requires detailed investigation. [1] aureus induced septic arthritis in rabbits. [2] aeruginosa-induced septic arthritis were investigated. [3] Salmonella induced Septic Arthritis is relatively rare in an immunocompetent child. [4]

induced septic ali

The results of hematoxylin and eosin, respiratory function detection, malondialdehyde level and superoxide dismutase activity determination and ELSIA demonstrated that taurine significantly alleviated lung injury, restored respiratory function, reduced oxidation and decreased the concentrations of inflammatory factors in CLP-induced septic ALI model rats. [1] Conclusion miR-144−3 can promote LPS induced septic ALI through downregulating Caveolin-2 to activate the JAK/STAT signal pathway. [2] However, we do not know whether it has a protective effect against CLP (cecal ligation and puncture)-induced septic ALI. [3]

induced septic injury

OBJECTIVE The aim of this study was to explore the role of alprostadil (Alp) in cecal ligation and puncture (CLP)-induced septic injury in rats and its possible mechanism of action. [1] Multispectral optoacoustic imaging showed that cecal ligation and puncture (CLP)-induced septic injury caused impaired renal excretion, which was improved in DHHC21 functional deficient (Zdhhc21dep/dep) mice. [2] Multispectral optoacoustic imaging showed that cecal ligation and puncture (CLP)-induced septic injury caused impaired renal excretion, which was improved in DHHC21 functional deficient (Zdhhc21dep/dep) mice. [3]

induced septic aki

We showed an activation of RIP3, accompanied by an accumulation of the autophagosome marker LC3II and the autophagic substrate p62, in the kidneys of lipopolysaccharide (LPS)-induced septic AKI mice and LPS-treated cultured renal proximal tubular epithelial cells (PTECs). [1] Furthermore, fisetin effectively reduced the number of TUNEL positive apoptotic cells and suppressed apoptotic protein of Bcl-2, BAX and cleaved caspase-3 in the kidneys of LPS-induced septic AKI. [2]

induced septic cardiac

Although epoxyeicosatrienoic acids (EETs) have multiple protective effects against different diseases, whether they can improve the pathogenesis of lipopolysaccharide (LPS)-induced septic cardiac dysfunction remains unknown. [1] Furthermore, a total of 10 hub genes NDUFB5, TIMMDC1, VDAC3, COQ10A, MRPL16 (mitochondrial ribosomal protein L16), C3orf43, TMEM182, DLAT, NDUFA8, and PDHB (pyruvate dehydrogenase E1 beta subunit) in the blue module were identified at transcriptional level and further validated at translational level in myocardium of an lipopolysaccharide-induced septic cardiac dysfunction mouse model. [2]

induced septic model

Mice pretreated with NTS intraperitoneally displayed improved survival rate and extended survival time in LPS‐ and polymicrobe‐induced septic models, respectively. [1] In our previous work, we found cannabinoid receptor Ⅱ(CB2R) inhibited the expression of HMGB1 in lipopolysaccharide (LPS)-induced septic models in vivo and in vitro, but the underlying mechanism is still unclear. [2]

induced septic death

Importantly, the pharmacologic inhibition of the AGER-ALOX5 pathway or global depletion (Ager−/−) or conditional depletion of AGER in myeloid cells (AgerMye−/−) protects against lipopolysaccharide-induced septic death in poly(I:C)-primed mice. [1] Moreover, C-23, administered at a clinically well-tolerated dose, inhibits LPS-induced septic death and IL-1β secretion in mice. [2]

induced septic response

Our study illustrates an example of drug repositioning of Biapenem (BIPM), a carbapenem antibiotic, for the modulation of HMGB1-induced septic responses. [1] This suppression of TGFBIp-mediated and CLP-induced septic responses indicates that collismycin C is a potential therapeutic agent for various severe vascular inflammatory diseases, with inhibition of the TGFBIp signaling pathway as the mechanism of action. [2]

induced septic lung

Here, we investigated the protective efficacy of protocatechuic acid (PCA) against lipopolysaccharide (LPS)-induced septic lung injury. [1] We found that the GFP expression pattern in the Hdc-GFP mice faithfully recapitulated that of conventional histamine-producing cells and that the GFP expression level mirrored the increased Hdc expression in lipopolysaccharide (LPS)-induced septic lungs. [2]

induced septic acute

Background This study sought to compare the therapeutic effects of angiotensin II (ANG II) and norepinephrine (NE) on cecal ligation and puncture (CLP)-induced septic acute kidney injury (AKI) in rats. [1] BACKGROUND We intended to investigate the function of circular RNA RasGEF domain family member 1B (circ_RASGEF1B) in lipopolysaccharide (LPS)-induced septic acute kidney injury (AKI) cell model and its associated mechanism. [2]