title: [CD38 protein reduces LPS/D-galactosamine-induced acute damage of liver tissues via down-regulating inflammatory cytokine expressions].
abstract: 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.
authors.affiliation: Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu 610041, China.
authors.forename: Yongqiang
authors.initials: Y
authors.lastname: Wu
authors.affiliation: Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu 610041, China.
authors.forename: Long
authors.initials: L
authors.lastname: Liang
authors.affiliation: Department of Rheumatology and Clinical Immunology, First Affiliated Hospital, Xiamen University, Xiamen 361005, China.
authors.forename: Guixiu
authors.initials: G
authors.lastname: Shi
mesh_terms: D051997:ADP-ribosyl Cyclase 1 / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D000208:Acute Disease; D000410:Alanine Transaminase / Q000097:blood / Q000276:immunology; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood / Q000276:immunology; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000235:genetics / Q000276:immunology*; D016207:Cytokines / Q000235:genetics / Q000276:immunology*; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000276:immunology*; D005688:Galactosamine; D015870:Gene Expression / Q000276:immunology; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D007274:Injections, Intraperitoneal; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology; D053583:Interleukin-1beta / Q000235:genetics / Q000276:immunology; D015850:Interleukin-6 / Q000235:genetics / Q000276:immunology; D008070:Lipopolysaccharides; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D011897:Random Allocation; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D005688:Galactosamine; D007371:Interferon-gamma; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D051997:ADP-ribosyl Cyclase 1