氧应激在大鼠乙醇及四氯化碳致慢性肝损伤中的作用

目的:复制大鼠乙醇及四氯化碳(CCl4)致慢性肝损伤模型,观察氧应激反应在其发生中的作用.方法:50只,♂ Wistar大鼠平均分为A-E 5组,实验持续8 wk.A组生理盐水灌胃;B组乙醇灌胃(560 mL/L);C组在B组基础上同时PGE1腹腔内注射;D组乙醇(560 mE/L,)灌胃4 wk,然后CCl4腹腔注射4 wk.E组在D组基础上同时PGE1腹腔内注射.实验4、8 wk结束时分别检测全血GSH-Px,血清ALT、AST、ALP、TBA、TG、CHO、MDA.8 wk结束时处死动物,留取肝脏标本,行光镜及电镜检查.结果:5组大鼠的原始体质量在统计学上无显著性差异,实验结束时,与A组相比,B组和D组的最终体质量和增加体质量明显降低(249.00 g±18.83 g,258.50 g±20.28 g vs319.00 g±29.61 g;65.00 g±15.28 g,76.50 g±15.82 g vs 134.00 g±21.58 g,均P<0.01),肝质量占体质量百分比明显增高(3.267%±0.3165%,4.735%±0.7567%vs2.736%±0.1988%.均P<0.01),相应PGE1干预后(C组和E组),大鼠的生长缓慢、肝脏肿大情况得到明显改善(均P<0.01);B组和D组血清中的ALT、AST、ALP、TBA、TG和CHO含量发生不同程度的升高(P<0.01或0.05),PGE1干预后增高水平明显下降;乙醇和CCl4能引起外周血GSH-Px降低和MDA升高(均P<0.01),PGE1干预后能够得到明显改善,而PGE1的干预则可明显减轻乙醇和CCl4引起的肝脏病理学改变.结论:氧应激反应可能在大鼠乙醇及CCl4致慢性肝损伤过程中发挥重要作用,抑制氧应激反应可能是缓解肝损伤的重要措施.

Role of oxidative stress in the pathogenesis of chronic hepatic injury induced by ethanol and carbon tetrachloride in rats

AIM:To investigate the role of oxidativ stress reaction in the pathogenesis of chroni hepatic injury induced by alcohol and carbon tetrachloride(CCl4 ) in rats.METHODS:Fifty male Wistar rats were di-vided equally into five groups:A, B, C, D and E.The experiment was continued for 8 weeks in each group.Groups A and B were perfused intragastrically with normal saline and alcohol, respectively.Group C was treated as group B and additionally injected intraperitoneally with prostaglandin E1(PGE1).Group D was perf...