心衰大鼠心肌细胞β2-AR的表达与心功能改变的关系及机制

Relationship between Expression of β_2-AR Protein on Cadiocyte and the Cardiac Function of Heart failure Rat

目的:探讨慢性心衰大鼠心肌细胞β2肾上腺素能受体(β2-AR)的表达变化,过表达β2-AR后心肌细胞收缩功能的改变及其可能机制。方法:通过腹主动脉缩窄术建立大鼠慢性心力衰竭(CCF)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β2-AR目的基因的重组腺病毒,通过免疫印迹方法检测正常细胞和心衰细胞β2-AR蛋白表达的变化,采用单个细胞动态边缘检测系统测定其收缩功能的改变。结果:与正常细胞相比,心衰时β2-AR蛋白的表达没有变化,转染β2-AR基因则使之表达增加(P<0.05)。与正常组相比,心衰组的基础收缩明显降低(3.955±1.684%vs5.472±2.918%,P<0.01);过表达β2-AR逆转了心衰心肌细胞的基础收缩(5.882±2.208%vs3.955±1.684%,n=60,P<0.01),但不影响心衰心肌细胞的最大收缩(9.366±2.646%vs9.066±3.509%)。结论:心衰时大鼠心肌细胞β2-AR的表达不变,但是其基础收缩功能降低,而β2-AR的过表达则能够改善心衰细胞的基础收缩功能。

Objective： To observe the changes of the expression of the β2-ARadrenergic （β2-AR） protein during the heart failure （CCF, HF）, and the function of cadiocyte after being transfected with Adv. β2-AR in rats. 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 its contractile function with IonOptix SoftEdge cell length acquisition systems. Results： Compared with sham group, the expression of the β2-AR protein of the failure cadiocyte did not changed in normal cadiocyte, which increased by transfection of β2-AR （P〈0.05）. Compared with the normal control group, the basal contraction amplitude of the failure cadiocyte was obviously decreased in the sham operated group （3.955 ± 1.684% vs 5.472±2.918%,P〈0.01）, but was turned over by Adv. β2-AR transfection （5.882±2.208% vs 3.955± 1.684%, P〈0.01）.The max contraction amplitude showed no difference between the group of sham and transfected group （9.366±2.646% vs 9.066±3.509%）. Conclusions： The expression of β2-AR protein in the failure cadiocyte did not changed, but its basal contraction amplitude decreased. The over-expression of the β2-AR protein could improve the function of the cadiocytes.