The Inhibitory Effect Of RHL On Myocardial Tissue Damage And Fibrosis In Hypertensive Rats

Objectives To establish the model of hypertensive rats by the method of “two Kindeyone Clip”,and to observe myocardial damage and fibrosis in rats,and to explore the inhibitory effect of RHL on the damage and fibrosis of myocardial tissue of hypertensive rats,and to clarify the possible mechanisms of the effect for providing data support and theoretical guidance for the related research.Methods 1 Modeling: 24 male SD rats were randomly selected from 32 male SD rats and then established hypertensive model.2 Grouping: 8 rats were in control group,18 rats were randomly selected from successful models,and they were randomly divided into model group,LY group and RHL group with 6 rats in each group.3 Testing:(1)Systolic blood pressure in rats of each group was measured before and four weeks,eight weeks and twelve weeks after modeling.(2)The left ventricular mass and heart mass in each group were measured,and the left ventricular tissue was extracted.(3)The histopathological changes of myocardium of rats in each group was observed by HE staining.Masson staining was used to detect the degree of myocardial fibrosis in rats of each group.(4)Western blot was used to detect the relative expression of collagen? and collagen?,inflammatory factors,p-Smad2 and p-Smad3 proteins in myocardium of rats in each group.(5)Relative expression of Smad7 protein in myocardium of rats in each group was detected by immunohistochemical staining.Results 1 SBP results: There was no significant difference in SBP among the groups before modeling(P>0.05);compared with the control group,SBP in the model group,LY group and RHL group increased significantly(P<0.05),but there was no significant difference in SBP among the model group,LY group and RHL group(P>0.05).2 Ratio of left ventricular mass to heart mass: Compared with the control group,the ratio of the model group was significantly higher(P<0.05);compared with the model group,the ratio of RHL group was significantly lower(P<0.05).3 HE and Masson staining results:Compared with the control group,the injury of myocardial tissue in the model group was significantly aggravated,accompanied by a large amount of collagen deposition;compared with the model group,the injury degree of myocardial tissue in HRL group was significantly reduced,and the amount of collagen deposition was significantly reduced.4Western blot results: Compared with the control group,the relative expression of collagen?and collagen?,inflammatory factors,p-Smad2 and p-Smad3 proteins in the myocardium of the model group increased significantly(P<0.05);compared with the model group,the relative expression of collagen? and collagen?,inflammatory factors,p-Smad2 and pSmad3 proteins in the myocardial tissue of rats in RHL group decreased significantly(P<0.05).5 Immunohistochemical staining results: Compared with the control group,the expression of Smad7 in myocardium of the model group was significantly decreased,there was statistical significance(P<0.05);compared with the model group,the expression of Smad7 in myocardium of rats in RHL group increased significantly(P<0.05).Conclusions 1 The hypertensive rat model was successfully constructed.From 4 weeks to 12 weeks after modeling,SBP among the model group,LY group and RHL group remained relatively stable.At 12 weeks after modeling,the degree of myocardial injury and fibrosis in hypertensive rats was obvious.2 RHL might alleviate myocardial injury in hypertensive rats;RHL might inhibit myocardial fibrosis in hypertensive rats.3 The expression of inflammatory factors in myocardium of hypertensive rats increased,theexpression of p-Smad2 and p-Smad3 increased,while the expression of Smad7 decreased.RHL may reduce myocardial injury and fibrosis in hypertensive rats by inhibiting the expression of inflammatory factors and inhibiting the TGF-?/Smads signaling pathway.Figure12;Table10;Reference 118...