慢性多重应激大鼠心房肌L-型钙通道α1c亚单位表达变化研究  

Downregulation of L-type calcium channel α1c subunit in myocardium with chronic multi-stress rats

作　　者：李福平[1] 肖颖彬[1] 马瑞彦[1] 陈林[1] 钟前进[1] 王学锋[1] 

机构地区：[1]第三军医大学新桥医院全军心血管外科中心,重庆400037

出　　处：《西部医学》2008年第4期686-688,692,共4页Medical Journal of West China

基　　金：全军医学科学技术研究"十一五"计划课题(NO.06H023);国际合作课题

摘　　要：目的研究慢性多重应激大鼠心房肌L-型钙通道α1c亚单位表达变化及L-型钙通道阻滞剂维拉帕米的拮抗作用。方法建立大鼠慢性多重应激心律失常模型,以维拉帕米作为干预,试验结束后取心房组织,用实时荧光定量反转录聚合酶链反应(real-time PCR)方法测定L-型钙通道α1c亚单位mRNA的表达水平,以Western blot方法检测L-型钙通道α1c亚单位蛋白的表达水平。结果应激大鼠出现了房性心律失常,应激+维拉帕米组房性心律失常出现时间和发生次数低于应激组(P<0.01);应激组和应激+维拉帕米组大鼠心房肌L-型钙通道α1c亚单位mRNA和蛋白表达水平明显低于对照组(P<0.01);应激组大鼠心房肌L-型钙通道α1c亚单位蛋白表达水平低于应激+维拉帕米组(P<0.01)。结论慢性多重应激导致大鼠心房肌L-型钙通道α1c亚单位mRNA和蛋白表达水平下调。维拉帕米对慢性多重应激诱导的大鼠心房肌L-型钙通道α1c亚单位表达下调有拮抗作用,可抑制慢性多重应激诱导的房性心律紊乱。Objective To study the downregulatlon of L-type calcium channel alc in atrial myocardium with chronic multl-stress rats and the antagonism effect of verapamil. Methods In this study, a chronic multi-stress animal model was established in rats. The animals were subjected to 4 weeks of chronic multi-stress. Verapamil was used to block L-type calcium channel. After 4 weeks, atrium tissue was harvested, the expression of L-type calcium channel alc was detected with RT-PCR and western blot. Results Expression of alc mRNA decreased in stress group compared with control group （P〈0. 01）. The same result was found in verapamil group compared with control group （P〈0.01）. There was no significant difference between stress group and verapamil group （P〉0. 05）. αlc protein expression was significantly reduced in stess group compared with control group （P〈0. 01）. There was a higher protein expression level in verapamll group than that in stress group （P〈0. 01）, which was lower than that in control group （P〈0.01）. Conclusion Chronic multi-stress induced a significantly decrease the expression level of L-type calcium channel αlc. Verapamil can attenuate L-type calcium channel αlc downregulation in chronic multi-stress model in rats.

关 键 词：应激 L-型钙通道 α1c 维拉帕米 

分 类 号：Q786[生物学—分子生物学] R654.2[医药卫生—外科学]