Ischemia reperfusion (I/R) injury is a key contributing factor to the pathogenic mechanism involved in cerebral infarction. Transmembrane protein 126b (TMEM126B), a mitochondrial complex I assembly factor, has been reported to have an intimate association with disease progression, but is little known in ischemia stroke. The present study was designed to explore the effects of TEME126B on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced neuronal PC12 cells. The mRNA level of TMEM126B was determined using qRT-PCR. The levels of ROS, MDA, and SOD, as well as inflammatory cytokines, were measured using corresponding commercial kits. Cell apoptosis rate was assayed by flow cytometry analysis, and the apoptosis-related proteins were measured using western blotting. ATP production measured by colorimetric reaction and mitochondrial membrane potential measured by JC-1 staining were conducted to determine mitochondrial dysfunction. The results showed that TMEM126B was upregulated upon I/R injury in vitro and in clinical, and was positively corrected with the degree of oxidative stress. TMEM126B knockdown significantly reduced oxidative stress and inflammation in OGD/R-induced PC12 cells. TMEM126B knockdown also attenuated cell apoptosis rate, accompanied with increased expressions of Bcl-2, XIAP and cleaved PARP-1, and decreased expressions of Bax, cleaved caspase 3 and cleaved caspase 9. Furthermore, TMEM126B knockdown exhibited cytoprotective roles through alleviating mitochondrial dysfunction, as assessed by ATP production and mitochondrial membrane potential. Collectively, this study indicates that TMEM126B knockdown protects against OGD/R-induced neuronal injuries through relieving oxidative stress, inflammation, apoptosis and mitochondria dysfunction, which provides a promising target for ischemic stroke treatment.

缺血再灌注（I / R）损伤是导致脑梗死的致病机制的关键因素。跨膜蛋白126b（TMEM126B）是一种线粒体复合体I组装因子，据报道与疾病进展密切相关，但在缺血性卒中中鲜为人知。本研究旨在探讨TEME126B对氧葡萄糖剥夺/复氧（OGD / R）诱导的神经元PC12细胞的影响。使用qRT-PCR确定TMEM126B的mRNA水平。ROS，MDA和SOD以及炎性细胞因子的水平使用相应的商业试剂盒进行测量。通过流式细胞术分析细胞凋亡率，并使用蛋白质印迹法测量凋亡相关蛋白。通过比色反应测量ATP的产生和通过JC-1染色测量线粒体膜电位，以确定线粒体功能障碍。结果表明，在体外和临床中，TMEM126B在I / R损伤后均被上调，并被氧化应激程度正向校正。TMEM126B组合件可显着降低OGD / R诱导的PC12细胞的氧化应激和炎症。TMEM126B敲低还减弱细胞凋亡率，并伴随Bcl-2，XIAP和裂解的PARP-1的表达增加，以及Bax，裂解的caspase 3和裂解的caspase 9的表达降低。此外，TMEM126B敲除通过减轻线粒体功能障碍发挥细胞保护作用，通过ATP产生和线粒体膜电位评估。总的来说，