Chen Xiao-lei, Tang Wan-Xin, Tang Xiao-hong, Qin Wei, Gong Meng
Department of Nephrology, West China Hospital, Sichuan University , Chengdu , China and.
Ren Fail. 2014 Sep;36(8):1298-303. doi: 10.3109/0886022X.2014.930650. Epub 2014 Jun 25.
Renal tubular epithelial cell injury is a major pathological event that contributes to the development of diabetic kidney disease (DKD). Uncoupling protein-2 (UCP2), a mitochondrial membrane protein, has been reported to participate in the regulation of reactive oxygen species (ROS) generation, which contributes to tubular cell apoptosis induced by hyperglycemia. In this study, we found that genipin, a UCP2 inhibitor, dramatically boosted oxidative stress, attenuated antioxidative capacity, and exacerbated cell apoptosis accompanied with caspase-3 activation in rat renal proximal tubular cells (NRK-52E) incubated with high glucose. The present study results suggest that manipulation of UCP2 could be important in the prevention of oxidative stress damage in renal tubular epithelial cells induced by hyperglycemia in vitro.
肾小管上皮细胞损伤是导致糖尿病肾病（DKD）发生的主要病理事件。解偶联蛋白2（UCP2）是一种线粒体膜蛋白，据报道其参与活性氧（ROS）生成的调节，这会导致高血糖诱导的肾小管细胞凋亡。在本研究中，我们发现UCP2抑制剂京尼平在高糖孵育的大鼠肾近端小管细胞（NRK-52E）中显著增强了氧化应激，减弱了抗氧化能力，并伴随着caspase-3激活加剧了细胞凋亡。本研究结果表明，调控UCP2对于预防体外高血糖诱导的肾小管上皮细胞氧化应激损伤可能具有重要意义。
