维生素E拮抗苯并[a]芘对雄性大鼠的肝脏毒性

Protective effect of vitamin E on benzo(a)pyrene (B[a]P)-induced liver toxicity in male Sprague Dawley rats

目的探讨维生素E(VE)对苯并[a]芘(B[a]P)诱导的雄性SD大鼠肝损害的作用及其机制。方法 60只4周龄的雄性SD大鼠随机分为空白对照组(未处理)、溶剂对照组(植物油)、单独染B[a]P组(5mg/kg)、VE低剂量组(10mg/kg VE+5mg/kg B[a]P)、VE中剂量组(50mg/kg VE+5mg/kg B[a]P)、VE高剂量组(100mg/kg VE+5mg/kg B[a]P)6组,每组大鼠10只。连续灌胃30d后,测定大鼠血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)的活性;测定肝脏组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性和8-羟脱氧鸟苷(8-OHdG)、丙二醛(MDA)、肿瘤坏死因子α(TNF-α)的含量;H-E染色观察大鼠肝脏组织形态结构。结果与对照组相比,单独染B[a]P组大鼠肝脏组织结构破坏,血清ALT和AST活性增加(P<0.05),8-OHdG、MDA和TNF-α含量升高,SOD、GSH-Px活性下降(P<0.05)。与单独染B[a]P组相比,VE各剂量组大鼠的肝脏组织损伤呈现不同程度的减轻,AST、ALT活性下降,8-OHdG、MDA、TNF-α含量降低,SOD、GSH-Px活性明显改善,差异均具有统计学意义(P<0.05);该效应具有剂量依赖性。结论 VE能拮抗B[a]P对雄性SD大鼠的肝脏毒性,起到肝脏保护作用。

Objective To investigate the protective effects of vitamin E （VE） on benzo（a）pyrene （B[a]P）-induced liver toxicity in male Sprague Dawley （SD） rats and to discuss the potential mechanisms involved. Methods Sixty male SD rats were randomly divided into 6 groups, namely, the blank control group, vehicle control group, B[a]P group （5 mg/kg）, VE （10 mg/kg） ＋ B[a]P （5 mg/kg） group, VE （50 mg/kg） ＋ B[a]P （5 mg/kg） group and VE （100 mg/kg） ＋ B[a]P （5 mg/kg） group, with each group having 10 rats. The rats were treated with B[a]P and/or VE once a day for 30 days via intragastric administration, and then the levels of alanine aminotransferase （ALT）, aspertate aminotransferase （AST）, superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px）, 8-hydroxy-2-deoxyguanosine （8-OHdG）, malondialdehyde （MDA） and tumor necrosis factor-α （TNF-α） were determined. The morphological changes of liver tissue were observed by H-E staining. Results Compared with the blank control group, the liver tissues in the B[a]P group were injured, the activities of serum AST, ALT, and the levels of MDA, 8-OHdG and TNF-a in B[-a]P group were increased significantly （P〈0. 05） ; however, the activities of SOD and GSH-Px were significantly decreased （P〈0. 05）. Importantly, rats in VE treatment groups had attenuated injury to liver tissues to different extents, decreased aminotransferase levels and greatly improved oxidative and DNA injury indicators. And with the increase of VE dose, the protective effect was more potent. Conclusion VE has a protective effect against the B[a]P-induced liver toxicity in male SD rats.