| Objective In essence,heart failure is a kind of overloading myocardiopath. The failure in myocardium reserve resulted in the deterioration of cardiac function. Much evidence indicated that with pathological stimulus of myocardium overload,the abnormal expression and regulation of a series of genes of cardiac myocyte has caused the expression change on some related gene and protein in myocardium,which resulted in the exhaustion of reserve-ability of myocardium. We studied some related gene protein that have something to do with proliferation,hyperplasia and apoptosis. The aim of this study of was to observe the myocardial expression of a -cardiac actin,G a11,p21,p27,p57,hhLIM,HCY-2 and HRG-1 etc in congestive heart failure rats models made by myocardial infarction during different period,and investigate the molecular biological mechanism of those protein in the evolution of myocardial hypertrophy and heart failure,so we should get a new method in clinical prevention and cure of myocardial hypertrophy and heart failure.Methods Rat CHF models were made by ligating the left coronary artery. In the state of heart failure in different period,the expression of a -cardiac actin,G a11 ,p21,p27,p57,hhLIM,HGY-2 and HRG-1 protein were assessed at 3D,1W,2W,3W,6W with immunohistochemistry,western bolting and image morphometry. The stage of rat CHF models was classfied acutemyocardial infarction(namely 3D),hypertrophy (namely 3W) and heart failure stage(namely 6W). Results1. The expression of a -cardiac actin protein put up the tendency namely from ascension to descent in the course of heart failure made by moycardial infarction. (1) Western Blot analysis:The densitometry values of a -cardiac actin ( at 3D,3W and 6W group of rat CHF models) were increased 24%(P<0.001),47%(P<0.001) and 12%(P<0.05) as compared with sham-operated rats,respectively,and the densitometry value of a -cardiac actin of 3W group in CHF model ( namely hypertrophy stage) was increased 20% (P<0.001) as compared with 3D group of CHF model (namely acute myocardial infarction stage),whereas the densitometry value of a -cardiac actin of 6W group in rat CHF model (namely heart failure stage) was significantly reduced 25%(P<0.001) as compared with CHF model group at 3W(namely hypertrophy stage). However,in the expression of a -cardiac actin protein,there were no outstanding difference in statistics test among control rats at 3D,3W and 6W(P>0.05). (2)Immunohistochemistry analysis (PU):the expression of a -cardiac actin protein of rat CHF model at 3 W was 1.34 fold (P<0.001) and 1.09(P<0.05) fold higher compared with 3D and 6W group of rat CHF models,respectively,and vs control group(P<0.01).2. The change of the expression of Ga M protein in the course of heart failure(Immunohistochemistry analysis):(1) The PU values of G a,,of CHF models at 1W,2W,3W were 1.17 fold(P<0.05),1.33 fold(P<0.01) and 1.97 fold(P<0.0001) higher as compared with control group,respectively,but the expression of G a,,protein was no outstandingstatistics difference between 3D and 6W group of rat CHF models(P> 0.05). (2) The PU value of G a of CHF model at 3W(namely hypertrophy stage) was 2.03 fold(P<0.0001) higher as compared with 3D group of CHF model(acute myocardial infarction),and The PU value of G a n of rat CHF model at 6W(namely heart failure stage) was significantly reduced 53%(P<0.0001) as compared with 3W group of rat CHF model.3. The expression of p21,p27 and p57 protein put up the tendency,namely from ascension to descent,in the evolution of heart failure made by myocardial infarction. Western Blot analysis:(1) the densitometry values of p21(at 3W and 6W group of rat CHF models) were increased 35%(P<0.001) and!6%(P<0.05) as compared with control rats,respectively,but the densitometry value of p21 of rat CHF model (at 3D) did not obviously increased as compared with control group (P>0.05). The densitometry value of p21 of 3W group in rat CHF model ( namely hypertrophy stage) was increased 30% (P<0.001) as compared with 3D group of CHF model... |
PDF Full Text Request