The mechanism of ginsenosides inhibiting myocardial autophagy in chronic heart failure rats through JAK/STAT signaling pathway
Objective:To investigate the mechanism of ginsenosides inhibiting myocardial autophagy in rats with chronic heart failure(CHF)through Janus kinase/signal transduction and transcriptional activator(JAK/STAT).Methods:65 male SD rats were randomly divided into control group,model group,ginsenoside Rb1 low-dose,medium-dose and high-dose groups.Rat CHF model was established,and 12 rats in each group were excluded.The control group and model group were given 10 ml/kg distilled water intragastric administration,and the other three groups were given 30 mg/kg,50 mg/kg and 70 mg/kg ginsenoside Rb1 intragastric administration once a day for 8 weeks.The cardiac function and hemodynamics of rats in each group were measured by ultrasound,and the myocardial tissue structure and cell apoptosis were measured by hematoxylin-eosin(HE)staining and TUNEL method.The expression of JAK/STAT pathway and Beclin1,microtubule-associated protein 1 light chain(LC3-Ⅱ)protein in myocardial tis-sue was detected by Western Blot.Results:Compared with the control group,the heart function and hemodynamics of the model group were decreased,and the heart function and hemodynamics of the ginsenoside Rb1 low,medium and high dose groups were increased compared with the model group(均 P＜0.05).In the model group,the myocardial tissue structure was incomplete,the cells were swollen and deformed,the boundary was blurred,the space was en-larged,the nucleus was shed,and a small amount of inflammatory cells were infiltrated.Ginsenoside Rb1 The struc-ture,cell boundary,size and arrangement of myocardium in low,medium and high dose ginsenoside Rb1 groups were gradually improved,which was better than that in model group.The apoptosis rates in control group,model group,ginsenoside Rb1 low,medium and high dose groups were(3.12±1.01)％,(34.04±8.76)％,(28.06±7.24)％,(18.05±5.13)％,(15.17±4.52)％(all P＜0.05).Compared with the control group,the protein expressions of JAK1,STAT3,Beclin1 and LC3-Ⅱ in the myocardium of the model group were increased,while the protein expres-sions of JAK1,STAT3,Beclin1 and LC3-Ⅱ in the myocardium of the ginsenoside Rb1 low,medium and high dose groups were successively decreased compared with the model group(均 P＜0.05).Conclusion:Ginsenoside Rb1 can protect cardiac function and regulate cardiomyocyte autophagy in CHF rats,and the mechanism may be related to the inhibition of JAK/STAT signaling pathway.
Chronic heart failureGinsenoside Rb1JAK/STAT signal pathCardiomyocytesHeart functionAutophagy
万方数据
维普
