临床儿科杂志 ›› 2014, Vol. 32 ›› Issue (1): 66-69.

• 专家笔谈 • 上一篇    下一篇

缝隙连接蛋白43在扩张型心肌病大鼠心肌中的表达及其与左室射血分数的相关性

袁勇华1 何学华1 方亦兵1 夏晓辉2   

  1. 湖南省人民医院 1. 儿科, 2. 超声科 (湖南长沙 410005)
  • 收稿日期:2013-08-11 出版日期:2014-01-15 发布日期:2014-01-15

Expression of connexin 43 in dilated cardiomyopathy and its correlation with left ventricular ejection fraction YUAN Yonghua1, HE Xuehua1, FANG Yibing1, XIA Xiaohui2 (1.Department of Pediatrics, 2.Deparment of Ultrasonography, Hunan People's Hospital, Changsha 410005, Hunan, China)

  • Received:2013-08-11 Online:2014-01-15 Published:2014-01-15

摘要:

 目的 探讨缝隙连接蛋白43(Cx43)在扩张型心肌病(DCM)模型大鼠左侧心室肌的表达及其与左心室射血分数(LVEF)的相关性。方法 应用多柔比星腹腔注射建立DCM大鼠模型;分别于造模成功当时(8周末)、造模4周后(12周末)检测正常对照组、DCM组的LVEF,留取左侧心室肌检测Cx43 mRNA表达和免疫组化观察Cx43的分布。结果 与对照组比较,DCM组在8周末、12周末Cx43 mRNA、Cx43平均灰度值及LVEF均明显下降,12周末下降最明显,差异均有统计学意义(P均<0.05)。Cx43 mRNA、平均灰度值与LVEF呈正相关(r=0.91、0.89,P均<0.01)。结论 DCM大鼠心肌Cx43表达明显减少且分布紊乱,Cx43可能参与了DCM的病理过程。

Abstract:  Objective To observe the expression of connexin 43 (Cx43) in left ventricular myocardium of rats with dilated cardiomyopathy (DCM) induced by adriamycin, and its correlation with left ventricular ejection fraction (LVEF). Methods The dilated cardiomyopathy model was established by intraperitoneal injection with adriamycin in Wistar rats. The LVEF of rats in DCM group and normal control group was investigated with echocardiogram at the end of the 8th week and 12th week, respectively. Meanwhile, myocardial Cx43 distribution was observed by immunohistochemical and image analysis techniques and Cx43 mRNA expression was tested by reverse transcriptase polymerase chain reaction (RT-PCR). Results Compared with the control group,the expressions of Cx43 protein (average gray value) and Cx43 mRNA and LVEF were all decreased significantly at the end of the 8th week and 12th week respectively in DCM group (P<0.05). The expressions of Cx43 protein and Cx43 mRNA in rat myocardium were positively correlated with LVEF (r=0.89 and 0.91, P<0.01). Conclusions Decreased expressions and heterogeneous distribution of Cx43 were observed in myocardium of rats in DCM model group. It is suggested that Cx43 may participate in the pathological process of DCM.