• Jing-Hui Chen, Gao-Feng Yu, Shang-Yi Jin, Wen-Hua Zhang, Dong-Xu Lei, Shao-Li Zhou, and Xing-Rong Song.
• Department of Anesthesiology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University Guangzhou 510630, People's Republic of China.
• Int J Clin Exp Patho. 2015 Jan 1; 8 (9): 10752-9.

AbstractSepsis induces hepatic injury but whether alpha-2 adrenoceptor (α2-AR) modulates the severity of sepsis-induced liver damage remains unclear. The present study used lipopolysaccharide (LPS) to induce hepatic injury and applied α2-AR agonist dexmedetomidine (DEX) and/or antagonist yohimbine to investigate the contribution of α2-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-1β, IL-6 & TNF-α), as well as a change in oxidative stress (MDA, SOD). Activation of α2-AR by dexmedetomidine (DEX) attenuated LPS-induced deleterious effects on the liver and block of α2-AR by yohimbine aggravated LPS-induced liver damage. Our data suggest that α2-AR plays an important role in sepsis-induced liver damage and activation of α2-AR with DEX could be a novel therapeutic avenue to protect the liver against sepsis-induced injury.

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