Effect and mechanism of maslinic acid on attenuating high glucose-induced myocardial cell injury and apoptosis

AIM To investigate the role of maslinic acid in high glucose-induced rat myocardial cell H9c2 apoptosis and possible mechanisms of action. METHODS High glucose-induced rat myocardial cell H9c2 model was constructed. Lactate dehydrogenase(LDH) release was used to test the degree of injury. TUNEL staining was used to detect the apoptosis. Western blot was used to detect the expression of AMPK, BCl-2 and Bax in H9c2 cells, and immunofluorescence assay was used to detect the reactive oxygen species(ROS) generation of myocardial mitochondria. RESULTS Compared with those in the control group, high glucose-treated cells exhibited a significant increase of LDH activity and apoptosis, whereas maslinic acid prevented the increase in high glucose-induced accumulation of LDH and decreased the degree of apoptosis. Western blot showed that the expression of p-AMPK and Bcl-2 decreased, but the expression of Bax increased in the high glucose group compared with those in the control group. Treatment with maslinic acid up-regulated p-AMPK and Bcl-2 and down-regulated Bax. However, Compound C, a special AMPK antagonist, reversed these effects induced by maslinic acid. Furthermore, ROS analysis revealed that maslinic acid inhibited high glucose-stimulated production of ROS, whereas pretreatment with AMPK antagonist compound C reversed maslinic acid and restrained ROS generation. CONCLUSION Maslinic acid exerts a protective effect on myocardium by activating AMPK, enhancing Bcl-2 expression and inhibiting Bax and ROS generation and high glucose-induced apoptosis.