Magnesium isoglycyrrhizinate improved myocardial remodeling through regulating oxidative stress and apoptosis
OBJECTIVE To explore the therapeutic mechanism of magnesium isoglycyrrhizinate(MgIG)for myocardial remodeling induced by isoproterenol(ISO)in mice.METHODS A total of 60 male mice of specific pathogen free(SPF)grade were assigned into 4 groups of blank control(control),positive control(control+MgIG),model(ISO)and treatment(ISO+MgIG).The serum contents of glutathione peroxidase(GSH-Px),creatine kinase isoenzyme(CK-MB),malondialdehyde(MDA)and lactate dehydrogenase(LDH)were detected by kits.The pathological changes of heart tissue were observed after hematoxylin-eosin(HE)/Masson stain.And the expressions of related proteins in heart tissue were detected by Western blot.RESULTS Serum detection,HE/Masson stain and protein expression indicated that ISO could cause myocardial injury in mice.As compared with control group,heart volume/mass,MDA,LDH,Collagen Ⅰ and phosphorylated phosphatidylinositol-3-kinase(p-PI3K)spiked in ISO group.The expressions of cleaved caspase-3 and phosphorylated protein kinase B(p-AKT1)were up-regulated(P＜0.05)while those of GSH-Px,Bcl-2,COX-2 and SOD1 down-regulated(P＜0.05).However,MgIG could reverse the cardiac damage of ISO and improve all parameters(P＜0.05).CONCLUSION MgIG can improve myocardial remodeling induced by ISO and its mechanism may be correlated with an inhibition of PI3K/AKT1 pathway for regulating apopto-sis and oxidative stress.It shall provide new rationales for clinical applications of MgIG on myocardial injury.
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