Aif Nuclear(艾夫核电)研究综述
Aif Nuclear 艾夫核电 - 7 macrophages including cell viability reduction; apoptosis generation; mitochondrial dysfunction; apoptosis-inducing factor (AIF) nuclear translocation; intracellular ROS generation; activation of the AMPK/Nrf-2/HO-1 pathway; changes in the expression of BCL-2 family proteins; and depletion of antioxidative enzymes (AOE), such as glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) These results indicate that 1-NP induced apoptosis in macrophages through AIF nuclear translocation and ROS generation due to mitochondrial dysfunction and to the depletion of AOE from the activation of the AMPK/Nrf-2/HO-1 pathway. [1] Furthermore, PAK5 phosphorylates AIF at Thr281 site to inhibit the formation of AIF/importin α3 complex, leading to decrease AIF nuclear translocation. [2] Further, NPD1 induced a reduction of mitochondrial BAX translocation and oligomerization, attenuated cytochrome C release and decreased AIF nuclear translocation. [3] Western blot and immunofluorescence were used to detect poly (ADP-ribose) polymerase-1 (PARP-1) activation and AIF nuclear translocation. [4] Neuroprotective effects of DML extracts were evaluated using relevant biochemical and imaging assays that measure cell viability/death, ROS generation, Ca2+ levels, mitochondrial dysfunction, and AIF nuclear translocation. [5]7个巨噬细胞，包括细胞活力降低；细胞凋亡的产生；线粒体功能障碍;凋亡诱导因子 (AIF) 核转位；细胞内 ROS 的产生； AMPK/Nrf-2/HO-1 通路的激活； BCL-2 家族蛋白表达的变化；和抗氧化酶 (AOE) 的消耗，例如谷胱甘肽过氧化物酶 (GPx)、过氧化氢酶 (CAT) 和超氧化物歧化酶 (SOD) 这些结果表明 1-NP 通过 AIF 核转位和线粒体功能障碍产生的 ROS 诱导巨噬细胞凋亡以及激活 AMPK/Nrf-2/HO-1 通路导致 AOE 的消耗。 [1] 此外，PAK5 磷酸化 Thr281 位点的 AIF 以抑制 AIF/importin α3 复合物的形成，导致 AIF 核转位减少。 [2] 此外，NPD1 诱导线粒体 BAX 易位和寡聚化减少、细胞色素 C 释放减弱和 AIF 核易位减少。 [3] Western印迹和免疫荧光用于检测聚（ADP-核糖）聚合酶1（PARP-1）活化和AIF核转位。 [4] DML 提取物的神经保护作用通过测量细胞活力/死亡、ROS 生成、Ca2+ 水平、线粒体功能障碍和 AIF 核转位的相关生化和成像分析来评估。 [5]
aif nuclear translocation Aif 核易位
7 macrophages including cell viability reduction; apoptosis generation; mitochondrial dysfunction; apoptosis-inducing factor (AIF) nuclear translocation; intracellular ROS generation; activation of the AMPK/Nrf-2/HO-1 pathway; changes in the expression of BCL-2 family proteins; and depletion of antioxidative enzymes (AOE), such as glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) These results indicate that 1-NP induced apoptosis in macrophages through AIF nuclear translocation and ROS generation due to mitochondrial dysfunction and to the depletion of AOE from the activation of the AMPK/Nrf-2/HO-1 pathway. [1] Furthermore, PAK5 phosphorylates AIF at Thr281 site to inhibit the formation of AIF/importin α3 complex, leading to decrease AIF nuclear translocation. [2] Further, NPD1 induced a reduction of mitochondrial BAX translocation and oligomerization, attenuated cytochrome C release and decreased AIF nuclear translocation. [3] Western blot and immunofluorescence were used to detect poly (ADP-ribose) polymerase-1 (PARP-1) activation and AIF nuclear translocation. [4] Neuroprotective effects of DML extracts were evaluated using relevant biochemical and imaging assays that measure cell viability/death, ROS generation, Ca2+ levels, mitochondrial dysfunction, and AIF nuclear translocation. [5]7个巨噬细胞，包括细胞活力降低；细胞凋亡的产生；线粒体功能障碍;凋亡诱导因子 (AIF) 核转位；细胞内 ROS 的产生； AMPK/Nrf-2/HO-1 通路的激活； BCL-2 家族蛋白表达的变化；和抗氧化酶 (AOE) 的消耗，例如谷胱甘肽过氧化物酶 (GPx)、过氧化氢酶 (CAT) 和超氧化物歧化酶 (SOD) 这些结果表明 1-NP 通过 AIF 核转位和线粒体功能障碍产生的 ROS 诱导巨噬细胞凋亡以及激活 AMPK/Nrf-2/HO-1 通路导致 AOE 的消耗。 [1] 此外，PAK5 磷酸化 Thr281 位点的 AIF 以抑制 AIF/importin α3 复合物的形成，导致 AIF 核转位减少。 [2] 此外，NPD1 诱导线粒体 BAX 易位和寡聚化减少、细胞色素 C 释放减弱和 AIF 核易位减少。 [3] Western印迹和免疫荧光用于检测聚（ADP-核糖）聚合酶1（PARP-1）活化和AIF核转位。 [4] DML 提取物的神经保护作用通过测量细胞活力/死亡、ROS 生成、Ca2+ 水平、线粒体功能障碍和 AIF 核转位的相关生化和成像分析来评估。 [5]