Study On The Effect And Mechanism Of Qiliqiangxin Capsule On Angiotensin Ⅱ-induced Ventricular Remodeling In Mice

Purpose:To establish the model of hypertensive ventricular remodeling by using the method of angiotension II perfusion,and to explore the effect and mechanism of Qiliqiangxin capsule on myocardial hypertrophy and myocardial fibrosis in hypertensive mice.Material and method:A mouse model of hypertensive ventricular remodeling was established by subcutaneous pump of angiotension II.C57 BL / 6 male mice of 8-10 weeks old were randomly divided into 4 groups,10 mice in each group,which were blank control group(distilled water gavage),Model group(distilled water gavage),Chinese medicine group(Qiliqiangxin 1g / kg · D gavage),Western medicine group(captopril 10 mg / kg · D gavage),and Ang Ⅱ stimulation was given at the same time.Blood pressure of mice was detected weekly;heart function of mice was detected before pump embedding,two weeks after pump embedding and four weeks after pump embedding;heart tissue morphology of mice in each group was observed by HE staining;myocardial fibrosis of mice in each group was observed by Masson and Sirius red staining;CD68,IL-6 and collagen III in hearts of mice in each group were detected by immunohistochemistry;the expression of ANP and BNP m RNA was detected by RT-PCR;and the expression of AT1 R,ERK1 / 2,p-ERK1 / 2,TGF-β 1,p-smad3 protein was detected by Western blot.Results:1.Blood pressure and cardiac function One week after Ang Ⅱ intervention,the blood pressure in Model group was significantly higher than that in the blank control group,then the blood pressure in Chinese medicine group and Western medicine group was significantly lower than that in Model group.After 2 weeks of Ang Ⅱ intervention,the EF value of mice in Model group was significantly lower than that in the blank control group,and the EF value of mice in Chinese medicine group and Western medicine group was significantly higher than that in Model group.The trend of FS value was the same as EF value.2.Cardiac hypertrophy HE staining showed that the heart in Model group was significantly larger than that in the blank control group,and the heart weight,heart weight to body weight ratio also supported the above results.There was no significant cardiac hypertrophy inChinese medicine group and Western medicine group compared with Model group,and the heart weight,heart weight to body weight ratio also supported the above results.The m RNA levels of ANP and BNP in the myocardium of mice in Model group were significantly higher than those in the blank control group.The m RNA levels of ANP and BNP in the myocardium of mice in Chinese medicine group and Western medicine group were significantly lower than those in Model group.3.Myocardial fibrosis Masson and Sirius red staining showed that myocardial fibrosis in Model group was significantly higher than that in the blank control group,and that in Chinese medicine group and Western medicine group was less than that in Model group.Immunohistochemical staining showed that compared with the blank control group,the expression of collage III was increased in Model group,and only a small amount of collage III was found in Chinese medicine group,Western medicine group than Model group.4.Inflammation in myocardial tissue CD68 and IL-6 were observed by immunohistochemistry.Compared with the blank control group,there were more brownish yellow granules in Model group,and only a few brownish yellow granules in Chinese medicine group and Western medicine group.5.Expression of AT1 R,ERK1 / 2,p-ERK1 / 2,TGF-β 1,p-smad 3 protein in myocardium Western blot showed that the expression of AT1 R,p-ERK1 / 2,TGF-β 1,p-smad 3 protein was higher in Model group than that in blank control group,Compared with Model group,the expression of AT1 R,p-ERK1 / 2,TGF-β 1,p-smad 3 protein in Chinese medicine group and Western medicine group decreased.Conclusion:1.Qiliqiangxin capsule can improve myocardial hypertrophy and fibrosis in mice,and its effect is similar to that of captopril.2.Qiliqiangxin capsule may improve the cardiac hypertrophy induced by Ang Ⅱ by down regulating AT1 R,and then down regulating p-ERK1 / 2 activation,and also improve the myocardial fibrosis induced by Ang Ⅱ by down regulating AT1 R,and inhibiting the activation of TGF-β 1 / Smad3 pathway.