摘要
目的:研究小分子活性肽apelin-13对尼古丁诱导的心肌细胞凋亡的作用,探讨其可能的调节机制。方法:建立尼古丁诱导的大鼠H9c2细胞凋亡模型,流式细胞术检测细胞凋亡率,Western blot法检测凋亡相关蛋白的表达。结果:(1)与正常对照组相比,尼古丁组细胞凋亡率明显增加(P<0.01),凋亡相关蛋白Bax和cleaved caspase-3的表达显著上调, Bcl-2、p-Akt、p-PI3K和APJ蛋白的表达显著下调(P<0.01);(2)与尼古丁组相比,apelin-13+尼古丁组细胞的凋亡率明显降低(P<0.01),Bax和cleaved caspase-3的表达显著降低(P<0.01), Bcl-2、p-Akt、p-PI3K和APJ蛋白的表达显著升高(P<0.01);(3)与apelin-13+尼古丁组相比,apelin-13+尼古丁+PI3K/Akt抑制剂LY294002组细胞凋亡率明显增加(P<0.01),Bax和cleaved caspase-3的表达显著增加(P<0.01), Bcl-2、p-Akt和p-PI3K蛋白的表达显著下调(P<0.01)。结论:Apelin-13通过PI3K/Akt信号通路抑制尼古丁诱导的H9c2细胞凋亡。
AIM: To investigate the effect of apelin-13 on nicotine-induced apoptosis of cardiomyocytes and its potential molecular mechanism. METHODS: Rat H9 c2 cells were treated with nicotine(10 μmol/L) to induced apoptosis. Flow cytometry was used to detect apoptotic rate. Western blot was used to determined the expression of related proteins. RESULTS: Compared with control group, nicotine treatment significantly increased the apoptotic rate of the H9 c2 cells(P<0.01), and the protein levels of apoptosis-related proteins Bax and cleaved caspase-3, but markedly decreased the protein levels of Bcl-2, p-Akt, p-PI3 K and APJ(P<0.05). Compared with nicotine group, apelin-13+nicotine significantly decreased the apoptotic rate of the H9 c2 cells(P<0.01) and the the protein levels of Bax and cleaved caspase-3, but markedly increased the protein levels of Bcl-2, p-Akt, p-PI3 K and APJ(P<0.05). Compared with apelin-13+nicotine group, apelin-13+nicotine+PI3 K/Akt inhibitor LY294002 significantly increased the apoptotic rate of the H9 c2 cells(P<0.01) and the protein levels of Bax and cleaved caspase-3, but markedly decreased the protein levels of Bcl-2, p-Akt and p-PI3 K(P<0.05). CONCLUSION: Apelin-13 inhibits nicotine-induced apoptosis of H9 c2 cells through PI3 K/Akt signaling pathway.
作者
张海增
全慧
单晓琼
田秋云
张福坤
范小芳
龚永生
ZHANG Hai-zeng;QUAN Hui;SHAN Xiao-qiong;TIAN Qiu-yun;ZHANG Fu-kun;FAN Xiao-fang;GONG Yong-sheng(Institute of Hypoxia Medicine, Wenzhou Medical University, Wenzhou 325035, China)
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2019年第8期1352-1358,共7页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.81370171)
浙江省医药卫生科学研究基金资助项目(No.2006B106)
