| Objective: Pathological models of congestive heart failure (CHF) were established by constricting the abdominal aorta of rats partly.The paper focused on the change of cardiac fun- ction, mitochondrial transmembrane potential, cardiomyocyte apoptosis and the protein expression of apoptosis-related gene Bcl-2 and Bax in pressure overload-induced CHF rats. Also it discussed the interventional role of captopril and XinfuKang Koufuye in the generation and development of the heart failure and the possible mechanism.Methods: By constricting the abdominal aorta of rats partly, the models of congestive heart failure were established. 80 SD rats were divided into four groups randomly:Sham opera- tion(SH),Coarctation of abdominal aorta model group (CAA),Captopril Tablets cure group(CAP) and XinfuKang Koufuye group(XFK)(n=20 each). In CAP group, the rats were treated with 10mg.kg-1.d-1 captopril, which was dissolved to 4ml with physiological saline, and gavaged respectively at the end of the first week after opration once a day. In XFK group, the rats were treated with 10mg.kg-1.d-1 XinfuKang Koufuye, which was dissolved to 4ml with physiological saline once a day. While in SH group and CAA group, the rats were treated with equal volume of physiological saline by the same way. And then the rats were measured the parameters of cardiac function (HR, SAP, DAP, LVMI, LVEDP,±dp/dtmax etc.) at the 6th week and 10th week respectively. At the same time, by using flow cytometry, the rats were measured the change of mitocho- ndrial membrane potential with rhodamine-123 fluorescence probe and the early myocardial apoptosis rate with AnnexinV- FITC/PI kit. as well as, determined the protein expression of apoptosis-related gene Bax and Bcl-2 with Bax, Bcl-2 monoclonal antibody.Result: 1 The change of cardiac function in each group:The results showed that, compared with SH group, SAP, DAP, HR, LVEDP, LVMI obviously increased(P<0.01), +dp/dtmax, -dp/dtmax significantly decreased(P<0.01) in CAA group at 6w and 10w. Compared with CAA group, SAP, DAP, HR, LVMI, LVEDP was significantly lower(P<0.01) and +dp/dtmax, -dp/dtmax was significantly higher(P<0.01) in CAP group and XFK group. Compared with CAP group, all kinds of cardiac function parameters in XFK group had no statistical signifycance(P>0.05). Compared with the cardiac function at 6w, there was no significant change in SH group at 10w(P>0.05). In CAA group, LVMI, LVEDP increased (P<0.05), +dp/dtmax,-dp/dtmax signifycantly decreased at 10w(P<0.01). In CAP group, HR, LVMI, SAP, LVEDP declined(P<0.05), -dp/dtmax increased(P<0.05), +dp/dtmax signifycantly increased(P<0.01). while in XFK group, HR, LVMI, LVEDP decreased(P<0.05), +dp/dtmax significantly increased (P<0.01), -dp/dtmax was no significant change (P>0.05). 2 The change of cardiomyocyte apoptosis and MMP in each group:The results showed that the apoptosis rate in CAA group was significantly higher(P<0.01) and MMP was significantly lower(P<0.01) than SH group at 6w and 10w. Compared with CAA group, apoptosis rate signifycantly decreased (P<0.01)and MMP significantly increased (P<0.01) in CAP group and XFK group. Compared with the cardiomyocyte apoptosis and MMP at 6w the apoptosis rate significantly decreased(P<0.01)and MMP significantly incr- eased(P<0.01) in CAP group at 10w. There was no significant change in SH,CAA and XFK group at 10w(P>0.05).3 The change of the protein expression of Bcl-2,Bax and Bcl-2/Bax in each group:The results showed that the protein expression of Bcl-2 in CAA group was significantly lower(P<0.01), the protein expression of Bax was obviously higher(P<0.01) and Bcl-2/Bax ratio was significantly lower(P<0.01) than SH group at 6w and 10w. In CAP group and XFK group, the protein expression of Bcl-2 obviously increased(P<0.01), the protein expression of Bax obviously decreased(P<0.01) and Bcl-2/Bax ratio significantly increased(P<0.01) than CAA group. Bcl-2 / Bax ratio was no difference between CAP group and XFK group (P>0.05). Compared with the protein expression of Bcl-2, Bax and Bcl-2/Bax ratio at 6w, Bcl-2/Bax ratio significantly decreased(P<0.01) in CAA group and significantly increased (P<0.01) in CAP group and XFK group. There was no significant change in SH group at 10w(P>0.05).Conclusion: 1 Coarctation of abdominal aorta can induce the CHF model, as time goes by, heart failure is more serious and cardiac function decreased in the CHF rats.2 Captopril can increase the expression of Bcl-2 protein, reduce the expression of Bcl-2 protein and increase Bcl-2/Bax ratio, stabilize mitochondrial membrane potential, prohibit cardiomyocyte apoptosis, reverse ventricular remodeling and improve heart function. 3 XinfuKang Koufuye can increase the expression of Bcl-2 protein, reduce the expression of Bcl-2 protein and increase Bcl-2/Bax ratio, stabilize mitochondrial membrane potential, prohibit cardiomyocyte apoptosis and treat CHF. |
