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目的:通过研究一氧化氮(NO)对小鼠急性重型肝炎病理改变的作用,以探讨重型肝炎的发病机理。方法:首先运用D-氨基丰乳糖(Galn)+细菌脂多糖(LPS),分不同时间建立小鼠急性重型肝炎模型,检测小鼠血清NO、血清丙氨酸转氨酶(ALT)、总胆红素(TBil),并观察肝组织的病理学政变。再观察运用NO供体左旋精氨酸(LArg)和NO合酶抑制剂左旋硝基精氨酸甲酯(L-NAME)对模型病变的影响。结果:①随着时间的延长小鼠血清ALT、TBil进行性升高,肝组织病理改变由细胞变性,点状坏死逐渐发展为广泛的肝细胞变性和大块出血坏死。不同时间组与正常对照组相比均有显著性差异。②在正常动物血清中有一定量的NO产生,模型建立后血清NO_2浓度随时间的延长呈上升趋势,至12h浓度可高达111.83μmol/L,与正常组相比有显著差异,且不同时间差异也有显著性。ALT、TBil的升高与NO之间具有明显相关性。③运用NO合成干预因素后,NO供体组血清NO_2升高,伴随ALT的上升和肝组织病变的加重;NOS抑制剂组NO_2水平降低、ALT水平下降,且肝组织损伤有一定程度的改善。结论:在Galn+LPS引起的肝损害中,小鼠体内NO生物合成机制被激活,NO参与了急性重型肝炎的发病,大量产生的NO表现为明显的肝组织损伤作用,是肝细胞损伤过程中的重要介质之一。运用L-NAME在一定程度?
Objective: To study the role of nitric oxide (NO) in the pathological changes of acute severe hepatitis in mice to explore the pathogenesis of severe hepatitis. Methods: The model of acute severe hepatitis was established at different time points by using Galn + LPS. The levels of NO, serum alanine aminotransferase (ALT), total bilirubin (TBil) and observe the pathological changes of liver tissue. The effect of NO donor L-arginine (LArg) and L-NAME, a NO synthase inhibitor, on the pathological changes of the model was observed. Results: ① With the prolongation of serum ALT and TBil in mice, the pathological changes of liver tissue were degenerated by cell degeneration and dot-like necrosis gradually developed into extensive hepatocellular degeneration and massive hemorrhagic necrosis. Different time groups compared with the normal control group were significantly different. ② There was a certain amount of NO production in normal animal serum. After the model was established, NO 2 concentration in serum increased with time, up to 111.83μmol / L at 12h, which was significantly different from that in normal group Significance. There was a significant correlation between elevated ALT and TBil and NO. ③ NO synthesis increased the NO 2 level in NO donor group, accompanied by the increase of ALT and the increase of liver tissue lesion. The NO 2 level decreased and the ALT level decreased in NOS inhibitor group, and the liver tissue injury improved to a certain extent. CONCLUSIONS: The mechanism of NO biosynthesis in mice is activated by Galn + LPS-induced liver injury. NO participates in the pathogenesis of acute severe hepatitis, and NO produced in large quantities shows obvious liver injury, One of the important media. Use L-NAME to a certain extent?