SIRT1 / 3, 莫诺苷, 心力衰竭, 氧化应激, 超氧化物歧化酶, 丙二醛

Objective To investigate the effect of morroniside on oxidative stress in heart failure rats induced by ligation of the left anterior descending coronary artery. Methods The rat model of heart failure was established by ligating the left anterior descending coronary artery and inducing myocardial infarction. The rats that survived the procedure were then divided into six groups: a model group, a low dose group of morroniside (60 mg / kg) , a medium-dose group of morroniside (120 mg / kg) , a high-dose group of morroniside (240 mg / kg) , captopril group (100 mg / kg) and the sham operation group was only threaded without ligation. Following a modelling period of 3 hours, the drugs were administered by gavage according to the corresponding drugs and dosage, once a day for a period of eight weeks. Hematoxylin eosin (HE) staining was used to detect the histopathological changes of the rat heart. The levels of SOD and MDA in the plasma of rats in each group were detected by WST-1 method and TBA method, respectively. Finally, Western blot analysis was used to detect the expression of SIRT1 and SIRT3 proteins in rat myocardium. Results Following a period of eight weeks, the result of HE staining demonstrated that, in comparison with the sham operation group, the myocardial cells in the model group exhibited a state of disarray, accompanied by the presence of broken and necrotic muscle fibers, as well as inflammatory cell infiltration. In comparison with the model group, the myocardial structure of rats in the morroniside group and captopril group was evidently enhanced and the infiltration of inflammatory cells was mitigated. The result of the SOD detection showed that the plasma SOD concentration in the model group was significantly lower than that in the sham operation group (P<0. 001) . In contrast, the morroniside group exhibited a significant increase in SOD concentration (P<0. 05,P<0. 01) , as did the Captopril group increased significantly ( P < 0. 01) . The result of the MDA test demonstrated that the concentration of MDA in the model group was significantly higher than that in the sham operation group (P< 0. 01) . In contrast, the morroniside group exhibited a significant decrease in MDA concentration (P<0. 05,P<0. 01) , and that in the Captopril group demonstrated a comparable decrease ( P<0. 01) .The result of the Western blot analysis demonstrated that the expression levels of SIRT1 and SIRT3 proteins in the model group were significantly lower than those in the sham operation group ( P<0. 05) . Compared with the model group, the expression level of morroniside in the High-dose group was significantly increased (P<0. 05) , and there was an increasing trend in the captopril group, though this was not statistically significant. Conclusion Morroniside may improve the oxidative stress injury in rats with heart failure subsequent to myocardial infarction by increasing the concentration of SOD in plasma, decreasing the concentration of MDA and Up-regulating the expression levels of SIRT1 and SIRT3 proteins, thereby reducing myocardial injury.

SIRT1 / 3;morroniside;heartfailure;oxidativestress;superoxidedismutase, malondialdehyde