重组腺病毒介导的BCL-X1基因过表达治疗急性肝衰竭大鼠的研究

目的明确肝细胞凋亡与急性大鼠肝衰竭模型肝组织损伤程度的关系;明确BCL—X1过表达对急性肝衰竭大鼠肝脏的治疗保护作用。方法将60只Wistar大鼠随机分为正常对照组、模型组、处理组三组。正常对照组及模型组给予门静脉注射生理盐水,处理组予门静脉注射重组BCL-Xl腺病毒。预处理7d后模型组及处理组予D-氨基半乳糖＋脂多糖建立肝衰竭模型,观察各组大鼠的BCL-X1蛋白的表达、ALT、AST水平、肝细胞凋亡率及死亡率。结果BCL．XI基因在处理组的表达高于在模型组中的表达;建立大鼠肝衰竭后6h,处理组的血清ALT、AST水平低于模型组（P〈0．05）。处理组的肝细胞凋亡率低于模型组（P〈0．05）。处理组的大鼠死亡率低于模型组（P〈0．05）。结论在急性肝衰竭大鼠中,肝细胞的凋亡率与大鼠的死亡率呈正相关;BCL-XI在肝组织中的过表达能减少急性肝衰竭模型大鼠的肝细胞凋亡率,降低急性肝衰竭大鼠的死亡率。

Adenoviruses mediated BCL-X1 overexpression protects mice from fulminant hepatic failure

Objective To indentify the relation between hepatic cells apoptosis and the lesion of liver tissue in acute toxic lethal hepatitis. Methods 60 Wistar mice were randomly divided into normal control, model group and treatment group. Normal control and model group were pretreated by portal vein injection of normal saline, the treatment group was pretreated by portal vein injection of BCL-X1 adenoviruses. The mice of model group and treatment group were received an injection of D-galn and LPS to establish fulminant hepatic failure models 7 days after pretrement. To observe BCL-XI expression, serum ALT, AST, hepatocyte apoptosis rate, and mortality rate of the three groups. Results The BCL-X1 expression was higher in treatment group than in model group;6 hours after fulminant hepatic failure models were established,the serum ALT,AST level of treatment group was lower than model group;The hepatocyte apoptosis rate of treatment group was lower than model group. The death rate of treatment group was lower than model group. Conclusion In fulminant mice hepatic failure models,the hepatocyte apoptosis rate has a positive correlation with death rate,the overexpression of BCL-X1 can decrease the hepatocyte apoptosis rate and the death rate.