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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12h的动态变化及肝组织iNOSmRNA的表达。结果试验组动物血清中ALT、AST进行性升高,在12h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12h时与对照组比较P<0.01。试验组动物肝组织细胞iNOSmRNA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iNOSmRNA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。
Objective To investigate the role of nitric oxide (NO) in acute severe hepatocytes injury induced by LPS (lipopolysaccharide) combined with GalN (D-galactosamine) in BALB / c mice. Methods At the same time, intraperitoneal injection of LPS and GalN saline solution in BALB / c mice served as the experimental group. The changes of ALT, AST and NO2 in serum were observed at 3, 6, 9 and 12 h, and the expression of iNOS mRNA in liver tissue was observed. Results The levels of ALT and AST in serum of experimental group increased progressively, and compared with the control group at 12h (P <0.01). NO2 in the serum of the experimental group showed a marked upward trend with time, compared with the control group at 12h (P <0.01). The expression of iNOS mRNA in liver tissue of experimental group increased continuously. The levels of ALT, AST and NO2- in the serum of the control group changed little, and the expression of iNOS mRNA was rare in the liver cells. Conclusion The mechanism of NO biosynthesis is activated in LPS combined with GalN-induced acute liver injury, which is one of the important mechanisms of hepatocyte injury.