Magnesium isoglycyrrhizinate regulates oxidative stress and apoptosis via PI3K/AKT1 pathway to improve myocardial remodeling in mice

Abstract

The role of magnesium isoglycyrrhizinate (MgIG) in myocardial remodeling is being investigated. We evaluated the result of MgIG on isoproterenol (ISO) -enticed myocardial remodeling in mice by activating the PI3K/AKT1 pathway. The heart function of mice was tested by echocardiography, and it was found that MgIG could improve the left ventricular function. Pathological staining analysis showed that MgIG could decrease the degree of myocardial injury caused by ISO. The serum data detected by ELISA showed that MgIG could reduce the content of CK-MB, MDA and LDH, and increase the activity of GSH-Px. Western blotting showed that the protein expressions of Collagen Ⅰ, BNP, Bax, Cleaved caspase-3, p-PI3K and p-AKT1 were decreased, while the protein expressions of Bcl-2, COX2 and SOD1 were increased. Meanwhile activation of the PI3K activator (740Y-P) reverses the cardioprotective effect of MgIG. These findings suggest that the myocardial remodeling induced by ISO could be improved by MgIG, and its mechanism may be associated with inhibite PI3K/AKT1 pathway to regulate apoptosis and oxidative stress.