Chen Hui, Huang Ri-Sheng, Yu Xian-Xian, Ye Qiong, Pan Lu-Lu, Shao Guo-Jian, Pan Jing
Department of Nephrology, Wenzhou Central Hospital, Wenzhou, Zhejiang 325000, P.R. China.
Department of Thoracic Surgery, Wenzhou Central Hospital, Wenzhou, Zhejiang 325000, P.R. China.
Exp Ther Med. 2017 Jul;14(1):447-452. doi: 10.3892/etm.2017.4473. Epub 2017 May 18.
The aim of the present study was to determine the effects of emodin, a natural compound with antioxidant properties, on oxidative stress and apoptosis induced by hypoxia/reoxygenation (H/R) in HK-2 human renal tubular cells. In HK-2 cells subjected to H/R, it was observed that pre-treatment with emodin lead to an increase in cellular viability and a reduction in the rate of apoptosis and the B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 ratio. H/R alone caused a significant increase in the levels of reactive oxygen species and malondialdehyde (P<0.05) and a significant decrease in the activities of superoxide dismutase, catalase and glutathione peroxidase (P<0.05), relative to normoxic cells. In turn, parameters of oxidative stress were improved by emodin pre-treatment. In addition, emodin pre-treatment significantly inhibited the phosphorylation of extracellular signal-regulated protein kinase and c-Jun N-terminal kinase mitogen-activated protein kinases (MAPKs) induced by H/R (P<0.05). These data suggest that emodin may prevent H/R-induced apoptosis in human renal tubular cells through the regulation of cellular oxidative stress, MAPK activation and restoration of the Bax/Bcl-2 ratio.
本研究的目的是确定大黄素（一种具有抗氧化特性的天然化合物）对HK-2人肾小管细胞缺氧/复氧（H/R）诱导的氧化应激和细胞凋亡的影响。在经历H/R的HK-2细胞中，观察到用大黄素预处理可导致细胞活力增加、细胞凋亡率降低以及B细胞淋巴瘤-2（Bcl-2）相关X蛋白/Bcl-2比值降低。相对于常氧细胞，单独的H/R导致活性氧和丙二醛水平显著升高（P<0.05），超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性显著降低（P<0.05）。反过来，大黄素预处理改善了氧化应激参数。此外，大黄素预处理显著抑制了H/R诱导的细胞外信号调节蛋白激酶和c-Jun N端激酶丝裂原活化蛋白激酶（MAPKs）的磷酸化（P<0.05）。这些数据表明，大黄素可能通过调节细胞氧化应激、MAPK激活和恢复Bax/Bcl-2比值来预防H/R诱导的人肾小管细胞凋亡。
