Activation of α2 adrenoceptor attenuates lipopolysaccharide-induced hepatic injury

Sepsis induces hepatic injury but whether alpha-2 adrenoceptor (alpha 2-AR) modulates the severity of sepsis-induced liver damage remains unclear. The present study used lipopolysaccharide (LPS) to induce hepatic injury and applied alpha 2-AR agonist dexmedetomidine (DEX) and/or antagonist yohimbine to investigate the contribution of alpha 2-AR in LPS-induced liver injury. Our results showed that LPS resulted in histological and functional abnormality of liver tissue (ALT and AST transaminases, lactate), higher mortality, an increase in proinflammatory cytokines (IL-1 beta, IL-6 & TNF-alpha), as well as a change in oxidative stress (MDA, SOD). Activation of alpha 2-AR by dexmedetomidine (DEX) attenuated LPS-induced deleterious effects on the liver and block of alpha 2-AR by yohimbine aggravated LPS-induced liver damage. Our data suggest that alpha 2-AR plays an important role in sepsis-induced liver damage and activation of alpha 2-AR with DEX could be a novel therapeutic avenue to protect the liver against sepsis-induced injury.