摘要
目的:探讨大鼠心肌细胞过表达2-AR后心肌细胞收缩功能的改变及其可能机制。方法:采用胶原酶消化法分离培养大鼠心肌细胞,转染携带β2-A目的基因的重组腺病毒,通过免疫印迹方法检测细胞β2-AR蛋白表达的变化,通过ELISA方法检测细胞中cAMP水平的改变,采用单个细胞动态边缘检测系统测定细胞收缩功能的变化。结果:与正常心肌细胞相比,β2-AR的转染增加了细胞上β2-AR蛋白的含量(P<0.05),并促进胞内cAMP水平的增加(14.763.15pmol/mlvs9.31.4pmol/ml,P<0.05);进而增强了心肌细胞的基础收缩(8.203±2.596%vs5.472±2.918%,P<0.01),但不改变最大收缩(9.128±2.852%vs9.366±2.646%)。结论:β2-AR的过表达能够增加细胞内cAMP水平并改善心肌细胞的收缩功能。
Objective： To observe the changes of contractile function of cadiocyte transfected with the Adv. GONG Hai-bin, LU Qian, WANG Jie, PANG Hui, WANG Lei β2-AR in rats. Methods： Rat cardiocytes isolated by collagenase II are transfected by Adv.GONG Hal-bin -AR for 48h, then the expression of β2-AR protein of cardioeytes was determined by immunoblotting and the levels of intracellular cAMP was detected through ELISA. The contractile function of these cells was observed with IonOptix SoftEdge cell length acquisition systems. Results： Compared with the control group, the expression of β2-AR protein ofcardiocytes and the level of the intracellular cAMP in Adv. β2-AR group were increased （P〈0.05）. The basal contraction amplitude of cadiocyte in Adv. β2-AR group was also increased significantly, but the max contraction of cardiocytes was not changed significantly between two groups （9.128± 2.852 % vs 9.366±2.646%）. Conclusions： The study suggested that the over-expression of β2-AR can increase the levels of intraeellular cAMP and improve the contractile function of cadiocytes in rats.
出处
《现代生物医学进展》
CAS
2009年第5期842-845,共4页
Progress in Modern Biomedicine
基金
国家自然科学基金资助项目(30572073)
江苏省自然科学基金项目(DK2005428)
江苏省医学重点人才(RC2007024)
江苏省"六大人才高峰"第三批项目(资金类型C)
