Vaspin prevents myocardial injury in rats model of diabetic cardiomyopathy by enhancing autophagy and inhibiting inflammation.

NLRP3 inflammasome activation plays an important role in diabetic cardiomyopathy (DCM). It is known that autophagy is related to the activation of inflammasomes during oxidative stress. Visceral adipose tissue-derived serine protease inhibitor (Vaspin), is an adipocytokine that has been shown to exert a protective effect on autophagic activity, but whether and how Vaspin improves myocardial damage in DCM remain unclear. In this study, we explored the role of Vaspin in DCM using a streptozotocin (STZ)-induced diabetes model. Cardiac function, cardiomyocyte apoptosis, myocardial tissue morphology, and mitochondrial morphology in diabetic rats were improved after eight weeks of Vaspin treatment. Vaspin treatment augmented autophagy activation in diabetic rat hearts. Moreover, the activation of NLRP3 inflammasome was inhibited by Vaspin, followed by a decrease in the cleavage of caspase-1 and maturation of IL-1β and TNF-ɑ. In vitro studies found that the mitochondrial reactive oxygen species (ROS) generation as well as the depolarization of the mitochondrial membrane in H9C2cells induced by high glucose were attenuated by Vaspin. This inhibitory effect of Vaspin on NLRP3 inflammasome activation was due to the protection of autophagy activity and was abolished after the treatment of autophagy inhibitor (3-MA). These results demonstrate that Vaspin alleviates STZ-induced myocardial injury and renders a cardioprotective effect by suppressing NLRP3 inflammasome activation and promoting autophagy.