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研究氧化苦参碱 (oxym atrine ,OM)对脂多糖 (LPS)加氨基半乳糖 (GalN)诱导的小鼠暴发型肝衰竭 (ful minanthepaticfailure ,FHF)的保护作用及其机理。实验分三组 :OM组 (10 0mgkg-1d-1× 3,ip) ,模型组及正常组。注射GaIN/LPS后 7.5小时 ,检测小鼠血清丙氨酸氨基转移酶 (ALT)和肿瘤坏死因子α(TNF -α)水平 ,同时取肝组织作HE染色和Fas及其配体 (FasL)的免疫组化检测。OM组小鼠ALT及TNF α水平明显低于模型组 (P <0 .0 1和 0 .0 5 )。OM组肝损害程度及Fas、FasL表达强度均较模型组减轻 (P <0 .0 1)。OM可能通过抑制TNF -α活性及Fas、FasL表达 ,从而阻断LPS所致肝细胞凋亡及坏死
To investigate the protective effect and mechanism of oxymatrine (OM) on fulminanthepaticfailure (FHF) induced by lipopolysaccharide (LPS) plus galactosamine (GalN) in mice. The experiment was divided into three groups: OM group (10 0mgkg-1d-1 × 3, ip), model group and normal group. Serum levels of alanine aminotransferase (ALT) and tumor necrosis factor α (TNF-α) were measured at 7.5 hours after injection of GaIN / LPS. Meanwhile, HE staining and Fas and Fas ligand Immunohistochemistry. The levels of ALT and TNFα in OM group were significantly lower than those in model group (P <0.01 and 0.05). The degree of liver damage and the expression of Fas and FasL in OM group were lower than those in model group (P <0.01). OM may inhibit the apoptosis and necrosis of hepatocytes induced by LPS by inhibiting the activity of TNF-α and the expression of Fas and FasL