Abstract：Abstract: Oxidative stress is one of the main pathogenesis of ischemic cardiomyopathy (ICM), and antioxidant is an important prevention strategy. In order to investigate the effects and mechanisms of taxifolin (tax) on the H2O2 induced oxidative stress, H9C2 cells were pretreated with/without tax (100 μmol/mL) for 6 h, and then exposed to hypoxia in the presence/absence of 200 μmol/mL H2O2 for the next 12 h. Oxidative stress level and autophagy phenomenon were evaluated by planar morphology, intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) generation, autophagosome and phagophore formation, and autophagy related proteins p62 and LC3 I/II expression levels. In order to reveal the possible molecular mechanisms, the expression levels of nuclear factor erythroid 2-related factor (Nrf2), hemeoxygenase-1 (HO-1), hypoxia-inducible factor 1α (HIF1α) were analyzed. The results showed that H2O2-induced H9C2 myocardial hypertrophy was inhibited by tax. At the same time, ROS and MDA productions were attenuated, Nrf2, HO-1 and HIF1α expressions were upregulated, and autophagy was promoted. In conclusion, the data suggests tax protects H9C2 cells from H2O2 induced oxidative stress via activation of Nrf2/HO-1/HIF1α/Autophagy pathway.
引用本文:
苏其利, 王晓莉, 谭小华, 陆亚朋, 旷寿金, 蔡 骞, 赵明一. 花旗松素通过激活Nrf2/HO-1/HIF1α/Autophagy信号通路对H2O2所致H9C2细胞氧化应激保护作用的研究[J]. 生命科学研究, 2017, 21(3): 233-238.
SU Qi-Li, WANG Xiao-Li, TAN Xiao-Hua, LU Ya-Peng, KUANG Shou-Jin, CAI Qian, ZHAO Ming-Yi. Taxifolin Protects H2O2-induced Myocardial Oxidative Stress via Activation of Nrf2/HO-1/HIF1α/Autophagy Pathway in H9C2 Cells. Life Science Research, 2017, 21(3): 233-238.
2017, Vol. 21 
