Regulating Tlr4(调节 Tlr4)研究综述
Regulating Tlr4 调节 Tlr4 - Conclusions: These above data suggest that NQO1 alleviates diabetes-induced renal inflammation and fibrosis by regulating TLR4/NF-κB and TGF-β/Smad signaling pathways. [1] In summary, our data suggest that miR-23b-5p promotes the chemosensitivity of TMZ via negatively regulating TLR4 in glioma, which provides a new therapeutic strategy for TMZ-resistant glioma treatment. [2] Collectively, OT exerted a beneficial effect on VILI by downregulating TLR4-and NLRP3-mediated inflammatory pathways. [3] Conclusions Ligustrazine nanoparticles had effective effects on Th1/Th2 balance by regulating TLR4/MyD88/NF-κB pathway in PPA rats. [4] In addition, miR-26a-5p overexpression decreased the contents of proinflammatory factors and inhibited cell apoptosis, while upregulation of TLR4 reversed these effects of miR-26a-5p mimics, implying that miR-26a-5p alleviated ALI by regulating TLR4. [5] MSNs led to high Ccl5/Cxcl9/Cxcl10 production in vitro and in mice through regulating TLR4-NFκB axis. [6] Conclusion These findings elucidated that circ-HACE1 contributed to the CSE-induced cell damages in COPD cell models via regulating TLR4 by acting as the sponge of miR-485-3p. [7] Whether propofol can act as an immunomodulator through regulating TLR4 are still unclear. [8] However, it is unclear whether miRNA can exert its neuroprotective effects by regulating TLR4-mediated inflammation. [9] Overall, we conclude that miR-224-5p may relieve AR by negatively regulating TLR4/MyD88/NF-κB pathway, indicating that miR-224-5p may be a promising target for AR treatment. [10] HSP90 in the spinal cord may be a co-stimulatory molecule for EA induced relief of neuropathic pain by regulating TLR4. [11] Overall, these aforementioned findings suggest that miR-16 may serve a protective role against LPS-mediated inflammatory responses in NHBE cells by regulating TLR4, where this mechanism may be considered to be a novel approach for treating ALI in the future. [12] This might be explained by IL-1ra downregulating TLR4-mediated NF-κB signaling pathway activation. [13] CONCLUSIONS RUS attenuated sepsis-induced ALI via protecting pulmonary endothelial barrier and regulating TLR4/Src/p120-catenin/VE-cadherin signalling pathway. [14] In conclusion, lncRNA PAPPA-AS1 might induce the development of HTS by upregulating TLR4 through interacting with TAF15. [15] Besides, miR-26a-5p overexpression decreased the contents of proinflammatory factors (TNF-α and IL-1β) and restrained cell apoptosis, while upregulation of TLR4 reversed these effects of miR-26a-5p mimics, implying that miR-26a-5p alleviated ALI through regulating TLR4. [16] We then found that further addition of heme or 5-aminolevulinic acid (ALA) increased heme biosynthesis and promoted inflammatory responses by upregulating TLR4/NF-κB and inflammatory cytokine expressions. [17] UTI attenuates LPS-induced inflammation and inhibits endoplasmic reticulum stress-induced apoptosis in renal tubular epithelial cells by regulating TLR4/NF-κB and Nrf2/HO-1 pathways. [18] In this study, oleuropein exhibited excellent anti-inflammatory effects by regulating TLR4-MyD88-NF-κB/MAPK axis in vitro and in vivo, suggesting oleuropein as a candidate molecule for treating AKI. [19] This study illustrated that EVs could carry miR‐129 to mitigate myocardial I/R injury via downregulating TLR4 and disrupting the NF‐κB signaling and NLRP3 inflammasome. [20] Therefore, IL‐10 alleviates LPS‐induced skin scarring via IL‐10R/STAT3 axis regulating TLR4/NF‐κB pathway in dermal fibroblasts by reducing ECM proteins deposition and the conversion of fibroblasts to myofibroblasts. [21]结论：以上数据表明，NQO1 通过调节 TLR4/NF-κB 和 TGF-β/Smad 信号通路减轻糖尿病引起的肾脏炎症和纤维化。 [1] 总之，我们的数据表明，miR-23b-5p通过负调节胶质瘤中的TLR4来促进TMZ的化学敏感性，这为TMZ耐药胶质瘤的治疗提供了新的治疗策略。 [2] 总的来说，OT 通过下调 TLR4 和 NLRP3 介导的炎症通路对 VILI 产生有益的影响。 [3] 结论川芎嗪纳米粒通过调节PPA大鼠TLR4/MyD88/NF-κB通路对Th1/Th2平衡具有有效作用。 [4] 此外，miR-26a-5p 过表达降低了促炎因子的含量并抑制了细胞凋亡，而 TLR4 的上调逆转了 miR-26a-5p 模拟物的这些作用，这意味着 miR-26a-5p 通过调节 TLR4 来缓解 ALI。 [5] MSNs 通过调节 TLR4-NFκB 轴在体外和小鼠体内导致高 Ccl5/Cxcl9/Cxcl10 产生。 [6] 结论 这些发现阐明了 circ-HACE1 通过作为 miR-485-3p 的海绵调节 TLR4 来促进 CSE 诱导的 COPD 细胞模型中的细胞损伤。 [7] 异丙酚是否可以通过调节 TLR4 作为免疫调节剂尚不清楚。 [8] 然而，尚不清楚 miRNA 是否可以通过调节 TLR4 介导的炎症来发挥其神经保护作用。 [9] 总体而言，我们得出结论，miR-224-5p 可能通过负调节 TLR4/MyD88/NF-κB 通路来缓解 AR，表明 miR-224-5p 可能是 AR 治疗的有希望的靶点。 [10] 脊髓中的 HSP90 可能是一种通过调节 TLR4 来缓解 EA 诱导的神经性疼痛的共刺激分子。 [11] 总体而言，上述研究结果表明，miR-16 可能通过调节 TLR4 对 NHBE 细胞中 LPS 介导的炎症反应发挥保护作用，这种机制可能被认为是未来治疗 ALI 的一种新方法。 [12] 这可以通过 IL-1ra 下调 TLR4 介导的 NF-κB 信号通路激活来解释。 [13] 结论 RUS 通过保护肺内皮屏障和调节 TLR4/Src/p120-catenin/VE-cadherin 信号通路减弱脓毒症诱导的 ALI。 [14] 总之，lncRNA PAPPA-AS1可能通过与TAF15相互作用上调TLR4来诱导HTS的发展。 [15] 此外，miR-26a-5p 过表达降低了促炎因子（TNF-α 和 IL-1β）的含量并抑制了细胞凋亡，而 TLR4 的上调逆转了 miR-26a-5p 模拟物的这些作用，这意味着 miR-26a-5p通过调节 TLR4 缓解 ALI。 [16] 然后我们发现进一步添加血红素或 5-氨基乙酰丙酸 (ALA) 通过上调 TLR4/NF-κB 和炎性细胞因子的表达来增加血红素的生物合成并促进炎症反应。 [17] UTI 通过调节 TLR4/NF-κB 和 Nrf2/HO-1 通路减弱 LPS 诱导的炎症并抑制内质网应激诱导的肾小管上皮细胞凋亡。 [18] 在这项研究中，橄榄苦苷通过在体外和体内调节 TLR4-MyD88-NF-κB/MAPK 轴表现出优异的抗炎作用，表明橄榄苦苷是治疗 AKI 的候选分子。 [19] 这项研究表明，EVs 可以携带 miR-129，通过下调 TLR4 和破坏 NF-κB 信号传导和 NLRP3 炎性体来减轻心肌 I/R 损伤。 [20] 因此，IL-10 通过减少 ECM 蛋白沉积和成纤维细胞向肌成纤维细胞的转化，通过 IL-10R/STAT3 轴调节真皮成纤维细胞中的 TLR4/NF-κB 通路来减轻 LPS 诱导的皮肤瘢痕形成。 [21]
Negatively Regulating Tlr4
In summary, our data suggest that miR-23b-5p promotes the chemosensitivity of TMZ via negatively regulating TLR4 in glioma, which provides a new therapeutic strategy for TMZ-resistant glioma treatment. [1] Overall, we conclude that miR-224-5p may relieve AR by negatively regulating TLR4/MyD88/NF-κB pathway, indicating that miR-224-5p may be a promising target for AR treatment. [2]总之，我们的数据表明，miR-23b-5p通过负调节胶质瘤中的TLR4来促进TMZ的化学敏感性，这为TMZ耐药胶质瘤的治疗提供了新的治疗策略。 [1] 总体而言，我们得出结论，miR-224-5p 可能通过负调节 TLR4/MyD88/NF-κB 通路来缓解 AR，表明 miR-224-5p 可能是 AR 治疗的有希望的靶点。 [2]