实用医学杂志2018，Vol.34Issue(4)：521-526,6.DOI:10.3969/j.issn.1006-5725.2018.04.002
CaMKII介导20-HETE诱导的乳鼠心肌细胞凋亡作用机制研究
A study on mechanisms of CaMKII mediated 20-HETE-induced apoptosis in neonatal rat cardiomyocytes
摘要
Abstract
Objective To study the effect of 20-HETE on apoptosis in cultured neonatal rat cardiomyo-cytes and investigate its mechanism. Methods Neonatal rat cardiomyocytes were cultured in vitro.CCK-8 method was used to detect the cell activity and TUNEL assay was performed to analyze the cell apoptosis. Flou-3/AM la-belled assay was applied to measure the concentration of intracellular calcium([Ca2+]i). Western blot was per-formed to measure the expressions of RyR2,SERCA2a,CaMKII and phospho-CaMKII. Results Treatment with 20-HETE reduced the activity of cardiomyocytes and induced cell apoptosis obviously,while KN-93,an inhibitor of CaMKII,blocked the effects of 20-HETE. Treatment with 20-HETE significantly increased cardiomyocytes [Ca2+]i,up-regulated the expression of RyR2,and down-regulated the expression of SERCA2a,which could be blocked by KN-93. 20-HETE also increased the expressions of CaMKII and phospho-CaMKII in cardiomyocytes, indicating 20-HETE played a role in activating the CaMKII signaling pathway. Conclusions 20-HETE leads to altered functions of cardiac sarcoplasmic reticulum calcium-transport protein RyR2 and SERCA2a via activating the CaMKII signaling pathway,which causes calcium overload and induces apoptosis in neonatal rat cardiomyocytes.关键词
20-羟二十烷四烯酸/CaMKII/细胞凋亡/钙超载Key words
20-HETE/CaMKII/apoptosis/calcium overload引用本文复制引用
贺滟,贾蝉忆,韩楚依,侯宏保,陈远寿,韩勇..CaMKII介导20-HETE诱导的乳鼠心肌细胞凋亡作用机制研究[J].实用医学杂志,2018,34(4):521-526,6.基金项目
国家自然科学基金资助项目(编号:81460040) （编号:81460040）
贵州省科学技术基金资助项目(编号:黔科合LH字[2014]7544号) （编号:黔科合LH字[2014]7544号）
