版权所有:内蒙古大学图书馆 技术提供:维普资讯• 智图
内蒙古自治区呼和浩特市赛罕区大学西街235号 邮编: 010021
作者机构:Beijing University of Chinese MedicineBeijing 100029China Fujian Medical UniversityFuzhou 350004China
出 版 物:《Journal of Traditional Chinese Medical Sciences》 (中医科学杂志(英文))
年 卷 期:2018年第5卷第3期
页 面:271-282页
学科分类:1006[医学-中西医结合] 1005[医学-中医学] 10[医学]
主 题:Hypoxia Yiqi Huoxue Decoction Chinese medicine Cardiomyocytes Oxidative stress
摘 要:Objective:Yiqi Huoxue Decoction (YQHX) has been widely used for clinical treatment of ischemic heart *** oxidative stress plays a key role in the pathogenesis of ischemic heart disease,the function and molecular mechanism underlying antioxidative protective effects of YQHX on H9c2 cardiomyocytes against ischemia/hypoxia (I/H) have yet to be well ***:H9c2 cells were subjected to 12 h of hypoxia with serum-free conditions and then treated with or without YQHX (100-400 μg/mL).Cell viability was examined using a CCK-8 *** dialdehyde (MDA) and superoxide dismutase (SOD) activity were detected using commercial *** reactive oxygen species (ROS) levels and mitochondrial membrane potential were measured using fluorescence microscopy and confocal laser-scanning microscopy,*** details of mitochondria in H9c2 cells were observed using transmission electron *** antioxidative protective pathway was assessed by measuring mRNA and protein expression of Nrf2 and HO-1,as well as AMPK ***:I/H injury gradually induced oxidative *** with YQHX significantly increased cell viability and reversed I/H-induced oxidative stress,including reducing the production of oxidative stress products (ROS and MDA),increasing SOD levels,improving mitochondrial morphology,and increasing mitochondrial membrane *** was also observed to increase I/H-induced expression of Nrf2 and HO-1,and the activation effects of YQHX were blocked by an AMPK *** addition,HPLC analysis showed that YQHX contained two active antioxidative constituents (calycosin and ferulic acid).Conclusion:The results suggest that anti-oxidative effects exerted by YQHX in H9c2 cardiomyocytes may be linked to upregulation of the AMPK-mediated Nrf2/HO-1 pathway.