Research on Effect of Ginsenoside Rb1 on Damaged Myocardial Cells by Regulating Calcium and Sodium Channels
Objective To investigate whether ginsenoside Rb1(Gs-Rb1)can alleviate doxorubicin(Dox)induced myocardial cell injury,and to determine whether the improvement effect of Gs-Rb1 on Dox myocardial cell injury is related to its regulation of sodium and calcium channels,and whether the AMP dependent protein kinase(AMPK)and/or calmodulin kinase Ⅱ(CaMKⅡ)pathways mediate this effect.Method Rat left ventricular myocardial cells were extracted and cultured.The cells were randomly divided into 7 groups:control group(PBS),Dox group,Gs-Rb1 group,AraA group,AraA+Gs-Rb1 group,KN93 group,KN93+Gs-Rb1 group.These groups were administered separately.ELISA method was used to detect the activities of N-terminal B-type natriuretic peptide precursor,AMPK and CaMKⅡ.DCFH-DA fluorescence probe assay was used to detect mitochondrial reactive oxygen species(mitROS)levels,and flow cytometry was used to detect intracellular reactive oxygen species(ROS)lev-els.Western blot was used to detect the expressions of total LTCC(t-LTCC),L-type voltage gated calcium channel(LTCC),ranidine receptor(RYR2),sarcoplasmic reticulum calcium ATPase(SERCA2a)and calcium sodium exchanger(NCX)proteins.Results The results showed that Gs-Rb1 significantly reduced the level of NT-proBNP in myocardial cells,which was signifi-cantly inhibited by AraA.Gs-Rb1 increased the AMPK activity of myocardial cells,which was completely inhibited by AraA and not affected by KN93.Gs-Rb1 reduced CaMKⅡ activity in myocardial cells.Gs-Rb1 reduced intracellular ROS and mitROS levels.Gs-Rb1 increased SERCA2a protein expression and reduced NCX expression.There was no statistically significant difference in tLTCC among the groups(all P＞0.05).Conclusion Gs-Rb1 reduces Dox induced NT-proBNP levels in myocar-dial cells,alleviating myocardial cell damage by regulating LTCC redistribution,enhancing RYR2 expression,increasing SERCA2a and inhibiting NCX.AMPK or/and CaMKⅡ pathways mediating this effect.Gs-Rb1 significantly inhibits Dox induced oxidative stress in cardiomyocytes,which can be mediated by the AMPK pathway and/or CaMKⅡ pathway.
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