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目的观察罗格列酮对D-GalN联合LPS诱导的小鼠急性肝衰竭的保护作用,并研究其可能的作用机制。方法选择雄性昆明小鼠60只,随机分为三组(正常组、对照组、治疗组),比较各组小鼠24h存活率,ALT,AST水平,肝组织病变程度(HE染色),RT检测各组小鼠肝组织中TNF-α、TGF-βl表达水平。结果 D-GalN 600mg/kg联合LPS10μg/kg腹腔注射成功构建了小鼠急性肝衰竭模型:24h存活率为20%;ALT,AST较正常组明显增高,P<0.05;病理学可见大面积肝组织坏死;肝组织中TNF-α、TGF-βl的表达均较正常组明显增高,P<0.05。结论罗格列酮对D-GalN/LPS小鼠急性肝衰竭有明显的保护作用,可改善肝细胞炎症和坏死,降低急性肝衰竭的死亡率,其机制可能与罗格列酮下调,TNF-α、TGF-βl的表达有关。
Objective To observe the protective effect of rosiglitazone on D-GalN combined with LPS-induced acute liver failure in mice and to explore its possible mechanism. Methods Sixty male Kunming mice were randomly divided into three groups (normal group, control group and treatment group). The survival rate, ALT and AST levels, liver pathological changes (HE staining) The expression of TNF-α and TGF-β1 in the liver tissues of mice in each group. Results The model of acute liver failure was successfully established by intraperitoneal injection of D-GalN 600 mg / kg and LPS 10 μg / kg: the survival rate of mice was 20% at 24 h; ALT and AST were significantly higher than those of normal group, P <0.05; Necrosis. The expression of TNF-α and TGF-β1 in liver tissue were significantly higher than those in normal group (P <0.05). Conclusion Rosiglitazone protects against acute liver failure in D-GalN / LPS mice, and can improve hepatocellular inflammation and necrosis and reduce the mortality of acute liver failure. The mechanism may be related to the down-regulation of rosiglitazone, α, TGF-βl expression.