不同剂量乙醇对大鼠血清抗氧化系统的动态影响及银杏黄酮的保护效应

目的研究不同剂量乙醇对大鼠血清抗氧化系统的影响及银杏黄酮的保护作用。方法雄性SD大鼠按体重随机分为正常对照组、低、中、高乙醇组(分别为0.8、1.6、2.4g/kg)和低、高干预组(48或96mg/kg银杏黄酮+2.4g/kg乙醇)和黄酮对照组(银杏黄酮96mg/kg)。试验D30、D60、D90取尾血测定血清还原型谷胱甘肽(GSH)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、丙二醛(MDA)活性或水平。结果大鼠摄入低剂量乙醇后,血清SOD、CAT和GSH-Px活性逐渐升高;摄入中剂量乙醇后,SOD与CAT在30d时升高,随后降至正常水平,而GSH水平在60、90d时明显下降,MDA水平持续升高;摄入高剂量乙醇后,实验期间抗氧化酶及GSH水平持续下降,MDA不断升高。银杏黄酮干预,尤其是在高剂量干预后,抭氧化酶失活与GSH消耗程度明显下降,MDA升高幅度也相应降低。结论低剂量乙醇摄入激活了机体的抗氧化系统,高剂量则导致严重的氧化应激;银杏黄酮对高剂量乙醇所致的氧化-抗氧化失衡有明显的调节和保护作用

THE DYNAMIC DOSE RESPONSE OF RAT SERUM ANTIOXIDANT SYSTEM TO ALCOHOL AND THE PREVENTIVE EFFECT OF GINKGETIN

Objective: To study the dynamic response of rat serum antioxidant system to ethanol with different doses and the protective role of ginkgetin on redox imbalance . Method: Male SD rats were divided into 7 groups according to their body weights, namely normal control, 3 ethanol groups at low, medium and high dose (0.8, 1.6, or 2.4 g/kg, respectively), low and high interventions (48 or 96 mg/kg ginkgetin 2.4 g/kg ethanol) and ginkgetin control (96 mg/kg). Serum was analyzed for the contents of glutathione (GSH) and malondialdehyde (MDA), as well as the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) on D 30, 60 and 90. Results: The activities of serum SOD, CAT and GSH-Px increased gradually in rats fed by low dose of ethanol. The activities of SOD and CAT were elevated on D 30, but GSH level decreased and MDA content increased gradually on D 60 and D90 when fed by medium ethanol. The inactive extents of serum antioxidant enzymes, including the degree of GSH depletion and MDA accumulation, were further increased in the presence of high ethanol. Ginkgetintreatment, especially at high dose, effectively inhibited the inactivation of antioxidant enzymes, depletion of GSH, and elevation of MDA level. Conclusion: Low ethanol activates the antioxidant defense system, whereas high ethanol results in evident redox disorder. Ginkgetin exerts favorable regulative and protective effect on the imbalance induced by high ethanol.