期刊文献+

依普利酮对棕榈酸诱导心肌细胞Cleaved caspase-3蛋白表达的影响 被引量:1

Effect of Eplerenone on the Expression of Cleaved Caspase-3 Protein in Cardiomyocytes Induced by Palmitic Acid
原文传递
导出
摘要 目的 探讨依普利酮(eplerenone,EPL)对棕榈酸(palmiticacid,PA)诱导心肌细胞Cleavedcaspase-3表达的影响。方法 以PA联合EPL处理乳鼠心肌细胞24 h,MTT法检测心肌细胞存活率,Westernblotting检测心肌细胞凋亡蛋白Cleaved caspase-3和自噬相关蛋白p62、LC3的表达水平。结果 与正常组比较,PA 200μmol·L-1刺激乳鼠心肌细胞24 h,细胞存活率明显下降(P<0.05);Cleaved caspase-3、p62和LC3Ⅱ/Ⅰ比值均显著上调(P<0.05);给予EPL处理后,与PA组比较,细胞存活率显著增加,上述蛋白表达水平显著降低(P<0.05)。结论 EPL通过影响心肌细胞内自噬,减轻脂毒性诱导的心肌细胞凋亡蛋白Cleaved caspase-3的表达。 OBJECTIVE To investigate the effect of eplerenone(EPL) on the expression of Cleaved caspase-3 in cardiomyocytes induced by palmitic acid(PA).METHODS Neonatal rat cardiomyocytes(NRCMs) were treated with PA and EPL for 24 h.The survival rate of cardiomyocytes was measured by MTT assay.The expression of apoptotic protein Cleaved caspase-3 and autophagy related proteins p62 and LC3 were detected by Western blotting.RESULTS Compared with the normal group,the survival rate of NRCMs was significantly decreased after being stimulated with 200 μmol·L-1 PA for 24 h(P<0.05),the expression of Cleaved caspase-3,p62 and the ratio of LC3 Ⅱ/Ⅰ in PA group were significantly increased(P<0.05).Compared with the PA group,the survival rate of NRCMs was significantly increased after treated with EPL,the above proteins expression were reduced(P<0.05).CONCLUSION Eplerenone can reduce the expression of Cleaved caspase-3 induced by lipotoxicity by affecting autophagy in cardiomyocytes.
作者 刘晓萍 梁关凤 欧阳资章 江晟 邓惠容 LIU Xiaoping;LIANG Guanfeng;OUYANG Zizhang;JIANG Sheng;DENG Huirong(Department of Pharmacy,The Sixth Affiliated Hospital of Guangzhou Medical University,Qingyuan People’s Hospital,Qingyuan 511518,China;Department of Pharmacy,Central People’s Hospital of Zhanjiang,Zhanjiang 524000,China)
出处 《中国现代应用药学》 CAS CSCD 北大核心 2022年第15期1938-1943,共6页 Chinese Journal of Modern Applied Pharmacy
基金 广东省医学科研基金项目(A2021149) 广东省中医药局科研项目(20222299)。
关键词 依普利酮 棕榈酸 自噬 心肌细胞 eplerenone palmitic acid autophagy cardiomyocytes
  • 相关文献

参考文献5

二级参考文献6

共引文献15

同被引文献7

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部