d-α-生育酚对乙醇引发的肝脏氧化应激的影响

目的观察d-α-生育酚对乙醇诱发的小鼠肝脏氧化应激的影响并探讨其机制。方法昆明种小鼠每天给予2.4g.kg-1bw乙醇后,再给予3个不同剂量的d-α-生育酚(25、50、100mg·kg-1bw.d-1),同时设正常对照组和乙醇对照组(乙醇2.4g·kg-1bw.d-1),连续灌胃60d后,测定肝脏超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、Na+,K+-ATP酶(Na+,K+-ATPase)、Ca2+,Mg2+-ATP酶(Ca2+,Mg2+-ATPase)、谷胱甘肽-S转移酶(GST)活力及丙二醛(MDA)的含量。结果小鼠摄入乙醇60d后,肝脏氧化应激水平明显增高。除Ca2+,Mg2+-ATPase以外,其余各项指标与正常对照组相比,差异均有显著性(P<0.05)。50mg·kg-1bw.d-1d-α-生育酚干预后,与乙醇对照组相比,GSH-Px、SOD、GST、Na+,K+-ATPase活力明显升高,MDA含量显著下降。其中,GSH-Px、Na+,K+-ATPase、MDA等3个指标在25mg·kg-1bw.d-1d-α-生育酚干预时亦出现同样的变化。结论适宜剂量的d-α-生育酚可以通过直接抑制脂质过氧化对乙醇诱发的肝脏氧化应激起保护作用。

The effect of d-α-tocopherol against ethanol-induced oxidative stress in mouse liver

Aim To investigate whether d-α-tocopherol supplementation had protective effect on the pro-oxidant-antioxidant state following chronic ethanol treatment in mouse liver and its underlying mechanism.Methods Mice were randomly divided into 5 groups:control(NC),ethanol control(EC),d-α-tocopherol 1(TOC 1),d-α-tocopherol 2(TOC 2)and d-α-tocopherol 3(TOC 3)group.After ingesting ethanol(2.4 g ethanol·kg-1 bw),the mice were treated by d-α-tocopherol(25,50,100 mg·kg-1 bw·d-1,respectively),meanwhile,the normal control group and ethanol control group(2.4 g ethanol·kg-1 bw)were set up.The activities of glutathione peroxidase(GSH-Px),superoxide dismutase(SOD),ATPase and glutathione-S transferase(GST)in liver were measured,meanwhile the concentration of malondialdehyde(MDA)was determined when the mice were continuously treated for 60 d.Results There was significant change in all indices between the ethanol control group and normal control group(P<0.05)except Ca2+,Mg2+-ATPase.The supplement of 50 mg·kg-1 bw·d-1 d-α-tocopherol could significantly prohibit the rise of MDA level and the decline of GSH-Px,SOD,Na+,K+-ATPase and GST activity induced by chronic alcohol intakes.The activity of Na+,K+-ATPase and GSH-Px were ameliorated by 25 mg·kg-1 bw·d-1 d-α-tocopherol,meanwhile,the rise of MDA level in liver was prohibited.Conclusion d-α-tocopherol might protect against ethanol-induced oxidative stress in mouse liver by directly quenching lipid peroxides,while excessive d-α-tocopherol showed no such benefits.