| Purpose:Through the establishment of Wistar rat heart failure model,the activities of AMPK,glyceraldehyde-3-phosphate dehydrogenase(GAPDH)and pyruvate kinase(PK)were detected to investigate the effect and mechanism of ginsenoside Rb1 on glycolysis and metabolism in heart failure ratsMaterial and method:(1)The experimental group used intraperitoneal injection of doxorubicin(Adr)for experimental animal modeling,and evaluated the model by echocardiography.(2)After successful modeling,the experimental group was randomly divided into six groups,namely heart failure control group,ginsenoside Rb1(Gs-Rb1)group,Ara-A-1 group,Ara-A-2 group,AICAR-1 Group and AICAR-2 group,then intraperitoneal injection of drug intervention.(3)Taking materials,using echocardiography,ELISA and spectrophotometry to determine the levels of adenylate activated protein kinase(AMPK),glyceraldehyde-3-phosphate dehydrogenase(GAPDH)and pyruvate kinase(PK)in each group Level.Results:1.The EF value of the Gs-Rb1 group,the AICAR-1 group and the AICAR-2 group was significantly higher than that of the heart failure control group(P <0.05),which was statistically significant,but there was no significant difference between the Gs-Rb1 group and the AICAR-2 group P> 0.05).The Ara-A-1 and Ara-A-2 groups and the heart failure control group had significantly lower EF(P = 0.000).The EF value of Ara-A-2 group and Gs-Rb1 group decreased(P <0.01)2 Compared with the control group,the AMPK activity of the heart failure control group was significantly increased(P = 0.000),and the Ara-A-1 and Ara-A-2 groups inhibited the AMPK activity of the rat compared with the heart failure control group(all P values ??were0.000),There is no statistical significance between the two(P> 0.05),Gs-Rb1 group and heart failure control group can increase AMPK activity in rats(P = 0.014).The AICAR-1 and AICAR-2 groups significantly increased the AMPK activity of rats(P <0.05),but no significant difference was found between the Gs-Rb1 group and the AICAR-2 group(P>0.05).3 The levels of pyruvate kinase and glyceraldehyde-3-phosphate dehydrogenase in heart failure rats were significantly higher than those in the control group(P <0.01);compared with the heart failure control rats,Ara-A-1 or Ara-A-There was no significant increase in the 2groups(P> 0.05),but the Ara-A-2 group was inhibited.However,the PK activity of the Gs-Rb1 group and the heart failure control group was significantly reduced(P <0.05),AICAR-1 and AICAR-2 The PK level of the group decreased significantly(P <0.05),and there was no significant difference between Gs-Rb1,AICAR-1 and AICAR-2(P> 0.05).Conclusion:1 Ginsenoside Rb1 improves the EF level of chronic heart failure in rats.2 Ginsenoside Rb1 can increase the activity of AMPK in rats.Ginsenoside Rb1 may partially depend on the AMPK pathway to improve heart failure in Wistar rats.3 Ginsenoside Rb1 reduces glycolytic enzyme activity in heart failure rats.Ginsenoside Rb1 may improve the energy metabolism of heart failure rats by regulating pyruvate kinase and glyceraldehyde-3-phosphate dehydrogenase in glycolysis. |
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