Adiponectin attenuates lipopolysaccharide-induced cell injury of H9c2 cells by regulating AMPK pathway.

Adiponectin, an adipokine synthesized and secreted majorly by adipose tissue, is reported to exert cardioprotective properties via anti-inflammation and antiapoptosis. Lipopolysaccharide (LPS) is a common inflammation and apoptosis inducer of cardiomyocytes. However, few studies have reported the roles of adiponectin on LPS-induced inflammation as well as apoptosis of H9c2 cells, and the possible mechanisms of these effects. In the present study, we found that adiponectin significantly relieved LPS-induced cytotoxicity including decreased viability and elevated LDH release, inhibited LPS-triggered inflammation, which is evidenced by increases in release of TNF-α, IL-1β as well as IL-6, and attenuated the enhanced rates of apoptotic cells as well as increased caspase-3 activity caused by LPS in H9c2 cells. In addition, our data demonstrated that adiponectin upregulated AMP-activated protein kinase (AMPK) activation of H9c2 cells with or without LPS administration. Moreover, we found that blocking AMPK pathway by compound c attenuated the protective effects of adiponectin against the cytotoxicity, inflammatory response, and apoptosis of H9c2 cells resulted from LPS. Our observations bring novel insights for understanding the mediatory role of AMPK pathway implicated in the protective effects of adiponectin against LPS-induced cardiotoxicity.