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目的:探讨大鼠原代培养肝细胞免疫性损伤模型病理特征,评价甘利欣(Grz)护肝作用。方法:用卡介苗(BCG)整体致敏,脂多糖(LPS)离体攻击(BCG+LPS)致肝细胞损伤。常规测AST,LDH活性,Griess法测NO含量;免疫细胞化学法测ICAM-1表达,丫啶橙荧光染色法和流式细胞仪测肝细胞凋亡率,评价Grz护肝作用。结果:LPS对上清AST无显著影响。BCG+LPS使上清AST,LDH,NO,肝细胞ICA8-1表达及凋亡率均明显高于正常对照组;Grz抑制AST和LDH的同时,使NO和12 h肝细胞凋亡率显著降低。氨基胍对NO也有显著抑制。结论:ICAM-1高表达,大量NO生成和肝细胞凋亡可能是BCG+LPS诱发大鼠原代肝细胞免疫性损伤的病理现象;Grz可显著抑制NO生成和肝细胞凋亡。
OBJECTIVE: To investigate the pathological characteristics of rat primary cultured hepatocellular autoimmune injury model and evaluate the role of Grz in protecting liver. Methods: Liver cell injury was induced by BCG sensitization and LPS challenge (BCG + LPS). AST, LDH activity and NO content were measured by Griess method. The expression of ICAM-1 was detected by immunocytochemical method. Apoptosis rate of hepatocytes was detected by acridine orange fluorescence staining and flow cytometry. Results: LPS had no significant effect on the supernatant AST. The expression of AST, LDH and NO, the expression of ICA8-1 in hepatocytes and the apoptosis rate of hepatocytes were significantly higher in BCG + LPS group than those in normal control group. Grz inhibited AST and LDH, and significantly reduced the apoptotic rate of NO and 12 h . Aminoguanidine also significantly inhibited NO. CONCLUSION: High expression of ICAM-1, massive production of NO and hepatocyte apoptosis may be pathological phenomena of primary hepatocyte immune damage induced by BCG + LPS in rats. Grz can significantly inhibit NO production and hepatocyte apoptosis.