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目的研究CD38蛋白在脂多糖联合D-氨基半乳糖(LPS/D-GalN)所诱发的小鼠急性肝损伤中的作用。方法野生型C57BL/6小鼠(WT)和CD38基因敲除小鼠(CD38 KO)随机分为正常对照组,模型早期组和模型晚期组。在造模后2 h和6 h处死动物,检测血清谷丙转氨酶(ALT)和谷草转氨酶(AST),实时荧光定量PCR检测肝脏组织炎症因子的表达,HE染色检测组织病理改变。结果在LPS/D-GalN诱导的模型小鼠中,与WT小鼠相比,CD38 KO小鼠血清ALT和AST水平显著升高,肝脏组织中炎性因子白细胞介素1β(IL-1β)、IL-6、肿瘤坏死因子α(TNF-α)以及γ干扰素(IFN-γ)的表达水平显著升高;病理组织学检测显示肝脏组织出血严重,肝实质细胞空泡变形明显增多,肝细胞死亡显著增加。结论 CD38蛋白通过下调炎症因子的表达,减少肝细胞死亡,减轻LPS/D-GalN诱导的急性肝脏损伤。
Objective To investigate the role of CD38 protein in acute liver injury induced by lipopolysaccharide and D-galactosamine (LPS / D-GalN) in mice. Methods Wild type C57BL / 6 mice (WT) and CD38 knockout mice (CD38 KO) were randomly divided into normal control group, early model group and late model group. Animals were sacrificed at 2 h and 6 h after model establishment. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured. The expression of inflammatory cytokines in liver tissue was detected by real-time fluorescence quantitative PCR. Histopathological changes were detected by HE staining. Results Compared with WT mice, the levels of ALT and AST in serum of CD38 KO mice were significantly increased in LPS / D-GalN induced model mice. The levels of inflammatory cytokines IL-1β, The expression of IL-6, TNF-α and IFN-γ were significantly increased. The histopathological examination showed that the hemorrhage of hepatic tissue was severe, the deformation of hepatocytes was significantly increased, Death increased significantly. Conclusion CD38 protein can reduce hepatic cell death and reduce acute liver injury induced by LPS / D-GalN by down-regulating the expression of inflammatory cytokines.