标题：Qiliqiangxin protects cardiac myocytes against hypoxia-induced apoptosis via ErbB4/PI3K/Akt pathway
作者：Zhou, Jingmin; Han, Xueting; Wang, Shijun; Fu, Mingqiang; Li, Zhiming; Ding, Xuefeng; Zhang, Jingjing; Qing, Chuhang; Li, Shuang; Ch 更多 作者机构：[Zhou, Jingmin; Wang, Shijun; Fu, Mingqiang; Hu, Kai; Zou, Yunzeng; Ge, Junbo] Fudan Univ, Shanghai Inst Cardiovasc Dis, Zhongshan Hosp, Dept Cardiol, 更多
通讯作者地址：[Ge, JB]Fudan Univ, Shanghai Inst Cardiovasc Dis, Zhongshan Hosp, Dept Cardiol, Shanghai, Peoples R China.
来源：INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
关键词：Qiliqiangxin; hypoxia; cardiac myocytes; apoptosis; ErbB4
摘要：Cardiac myocytes apoptosis played an important role in heart failure. Plenty of studies reported that Qiliqiangxin (QL), a traditional Chinese medicine, had therapeutic efficacy in chronic heart failure, but the underlying mechanism was not clear. Here we investigated whether QL prevented hypoxia-induced cardiac myocytes apoptosis and the possible mechanism. Isolated neonatal rat cardiac myocytes (NRCMs) were transfected by Lentiviral-ErbB4-siRNA, treated by a specific PI3K inhibitor (LY294002), and subjected to hypoxia with or without QL. Cell apoptosis was detected by terminal deoxynucleotide transferased UTP nick end labeling (TUNEL), flow cytometry and caspase-3 activity assay, respectively. ErbB4 mRNA level was detected by real-time PCR, protein expressions of ErbB4 and phosphorylated Akt were examined by Western blot. The results showed that hypoxia induced significant increase of apoptotic NRCMs, which was significantly attenuated by QL treatment. Further, QL induced the upregulation of ErbB4 and phosphorylation of Akt in hypoxic NRCMs. However, knocking down ErbB4 abolished these effects induced by QL. Furthermore, decrease of NRCMs apoptosis induced by QL was also abrogated by blocking PI3K/Akt signaling. Our data suggested that QL protected cardiac myocytes against hypoxia-induced apoptosis via regulating ErbB4-dependent PI3K/Akt pathway.