摘要
目的:检测过表达β_2-AR蛋白的慢性心衰大鼠心肌细胞SERCA2a/PLB的改变及相关信号转导通路的改变,初步探讨过表达β_2-AR基因影响心衰大鼠心肌细胞收缩功能的分子机制。方法:通过腹主动脉缩窄术建立大鼠慢性心力衰竭模型并采用胶原酶消化法分离心衰大鼠心肌细胞,转染携带β_2-AR目的基因的重组腺病毒,通过免疫印迹方法检测β_2-AR的过表达对心衰时SERCA2a/PLB的影响,及其导致的心肌收缩功能的改变,探讨过表达β_2-AR保护心衰大鼠心肌细胞的分子信号机制。结果:心衰后β_2-AR的过表达改善了PLB与SERCA2a的结合与解离,从而调节了SERCA2a对Ca^(2+)的摄取(P<0.05)。结论:心衰大鼠心肌细胞过表达β_2-AR后,增加的β_2-AR通过PLB/SERCA2a调节了心肌细胞的收缩舒张功能。
Objective： To detect the changes of SERCA2a/PLB and related signal transduction pathway of myocardial cells in rats with chronic heart failure by expressing β2-AR protein, explore the molecular mechanism of β2-AR gene over expression affect myocardial contractile function in rats with heart failure. Methods： The rat model of chronic heart failure was established by partially banding abdominal aorta and the cadiocyte was isolated with collagenase II, then the cadiocyte was transfected with Adv. β2-AR to observe the change of the key proteins during the myocardial contraction in Western Blot. Results： Overexpressed β2-AR protein modulated the expression of SERCA2a/PLB, and the congsistence of Ca^2＋ （P〈0.05）. Conclusions：The overexpressed β2-AR protein can make the cadiocyte antagonist the toxic actioni of heart failure throught the SERCA2a/PLB.
出处
《江苏科技信息》
2016年第30期42-47,共6页
Jiangsu Science and Technology Information
基金
市科技局社会发展项目
项目编号:XM13B043
徐州市社会发展项目
项目编号:XM12B062
江苏省临床医学科技专项
项目编号:BL2012019
