• Yongqiang Wu, Long Liang, and Guixiu Shi.
• Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu 610041, China.
• Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2014 Oct 1;30(10):1009-12.

ObjectiveTo investigate the role of CD38 in lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced acute hepatic injury in mice and explore the potential mechanism.MethodsA mouse model of acute hepatic injury was induced by an intraperitoneal injection (i.p.) of D-GalN and LPS. C57BL/6 wild-type mice (WT) and CD38 gene knockout mice (CD38 KO) were randomly divided into normal control group, early model group (2 hours after i.p. of LPS/D-GalN) and late model group (6 hours after i.p. of LPS/D-GalN), respectively. Two and six hours after administration of D-GalN/LPS, WT mice and CD38 KO mice were sacrificed, and the blood and liver tissue were collected. Serum was used to detect the alanine aminotransferases (ALT) and glutamate oxaloacetate transaminase (AST) levels. The injury of liver was assessed by HE staining. The expressions of IL-1β, IL-6, TNF-α and IFN-γ were analyzed by real-time quantitative PCR.ResultsCompared with the WT mice, CD38 KO mice presented significant increases of serum ALT and AST, mRNA expressions of IL-1β, IL-6, TNF-α and IFN-γ, as well as hepatocellular necrosis and bleeding in liver tissues after LPS/D-GalN induction.ConclusionCD38 protein effectively reduces the LPS/D-GalN-induced damage of liver tissues via depressing the expressions of inflammatory cytokines and inhibiting the death of liver cells.

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