[CD38 protein reduces LPS/D-galactosamine-induced acute damage of liver tissues via down-regulating inflammatory cytokine expressions].

OBJECTIVE

To investigate the role of CD38 in lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced acute hepatic injury in mice and explore the potential mechanism.

METHODS

A 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.

RESULTS

Compared 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.

CONCLUSIONS

CD38 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.