NO在小鼠急性重型肝损伤中的作用

目的探讨NO(一氧化氮)在LPS(脂多糖)联合GalN(D-氨基半乳糖)诱导BALB/c小鼠急性重型肝细胞损伤中的作用.方法同时腹腔注射LPS与GalN的生理盐水溶液于BALB/c小鼠作为试验组.观察血清中ALT、AST、NO2-在3、6、9和12 h的动态变化及肝组织iNOS mRNA的表达.结果试验组动物血清中ALT、AST进行性升高,在12 h时与对照组比较P＜0.01.试验组动物血清中NO2-随时间呈明显上升趋势,在12 h时与对照组比较P＜0.01.试验组动物肝组织细胞iNOS mRNA的表达不断增强.对照组血清中ALT、AST及NO2-含量变化不大,其肝细胞极少见iNOS mRNA的阳性表达.结论在LPS联合GalN所致急性肝损伤中,动物体内NO生物合成机制被激活,是其肝细胞损伤的重要机制之一.

Effect of NO on acute severe hepatic injury induced by integrative LPS and GalN

[Objective] Study effect of NO (Nitrogen monoxide) on acute severe hepatic injury induced by integrative LPS (lypopolysacchride) and GalN (D-galactosamine). [Methods] 56 male BALB/c mice were randomly divided into two groups. NS (normal saline, 0.2 mL) was injected intraperitoneally to be regarded as the control group.LPS (5 μg/kg) with GalN (800 mg/kg) together in NS was injected intraperitoneally to be served as the test group.Plasma samples for ALT, AST, NO2- measurements were obtained at 3,6,9 and 12h after respective treatments, meanwhile ISH detection of iNOS mRNA in hepatocyte. [Results] In the test group, the level of ALT, AST, NO2,- in plasma was ascending sharply (P ＜0.01, vs the control group at 12 h). By ISH detection, expression of iNOS mRNA in hepatocyte of liver tissue sections in the test group was enhancing continuously. There were little changes of ALT,AST, NO2- in plasma and expression of iNOS mRNA in iver tissue sections in the control group. [Conlusions] The biosynthetic mechanism of NO is triggered, and NO plays an important role in the acute severe hepatic injury induced by LPS and GalN together. NO may involve in the mechanism of the liver injury.