The Effect Of Wenxinkeli On Myocardial Hypertrophy And Connexin43in Rats

Objective: This study is to observe the effect of WXKL on the model ofmyocardial hypertrophy, which model was induced by norepinephrine (NE) in vitro,the observed index included cell morphology, proliferation rate and the expression ofConnexin43(Cx43). Then observe the effect of WXKL on the rat model of myocardialhypertrophy, which model was induced by pressure afterload in vivo, the observedindex included QT interval dispersion (QTd), myocardial remodeling and theexpression of Cx43.Methods: In vitro, H9c2myocardial cells were cultured, and then divided intonormal control group, NE group, WXKL group and NE+WXKL groups. Myocardialcell viability was measured by MTT after24hours. The myocardial cells diameter,cell protein content and the expression of Cx43were measured after72hours. In vivo,rats were divided into sham-operation (SO) group, abdominal aorta constriction (AC)group and abdominal aorta constriction+WXKL (AW) group. The rat model ofmyocardial hypertrophy was build by abdominal aortic constriction, and then fed withWXKL for12weeks. The cardiac function in rats were measured by cardiacB-ultrasound, the changes of QTd were detected by inserting homemade electrodesubcutaneously. Then put rat to death, and remove the heart. At last, the myocardialstructural remodeling was observed by HE staining, the distribution and expression ofCx43protein in the left ventricular myocardial tissue was measured byimmunohistochemistry, the expression of Cx43in the left ventricular myocardialtissue was detected by RT-PCR.Results:1) In vitro, the model of myocardial hypertrophy, induced by NE in vitro,was build successfully, and the study indicated that WXKL had no significant effecton the proliferation rate, cell protein content and the expression of Cx43mRNA innormal H9c2myocardial cells（P>0.05）, but it could confront the cytotoxic effect ofNE on myocardial cells, such as the inhibition of proliferation, the increase of the cell diameter and cell protein content, and the decreased expression of Cx43mRNA（P<0.05）.2) In vivo, the model of myocardial hypertrophy, induced by pressureafterload, was build successfully, and the study shown that WXKL could shorten theQT dispersion of rats with cardiac hypertrophy, improve myocardial remodeling andincrease the expression of Cx43（P<0.05）.Conclusions:1) WXKL could confront the cytotoxic effect of NE on H9c2myocardial cells, such as cardiomyocyte hypertrophy and the decreased expression ofCx43.2) WXKL could shorten the QT dispersion of rats with heart failure, improvemyocardial remodeling and increase the expression of Cx43in myocardial tissue.