【摘要】 目的:探讨长期口服卡托普利对小鼠脑组织自由基及相关酶的影响,为其临床应用提供实验依据。方法:取30只小鼠,随机均分为正常对照组(水)和卡托普利组(卡托普利,11.08～14.92mg·kg-1·d-1),按饮水给药方式连续给药14周,测定脑组织中自由基与相关酶(丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、钠-钾泵三磷酸腺苷酶(Na+-K+-ATP酶)、钙-镁泵三磷酸腺苷酶(Ca2+-Mg2+-ATP酶))水平。结果:与正常对照组比较,卡托普利组小鼠脑组织中MDA水平降低(P<0.05);SOD、GSH-Px水平均无明显变化;Ca2+-Mg2+-ATP酶、Na+-K+-ATP酶活性有降低的趋势,但无统计学意义。结论:长期口服卡托普利可减少脑组织自由基含量,增强机体抗氧化能力,但脑组织神经细胞膜功能有受损的可能。更多还原

【Abstract】 OBJECTIVE:To explore the effect of long-term oral dose of Captopril on free radicals and related enzymes of mice cerebral tissue in order to give experimental basis for clinical use of captopril.METHODS:30 normal adult mice were divided into control group(water)and captopril group(captopril 11.08～14.92 mg·kg -1 ·d -1 ).Both groups were given medicine for 14 weeks. Free radicals and the activity of related enzymes(MDA,SOD,GSH-Px,Na+-K+-ATP enzyme,Ca2+-Mg2+-ATP enzyme)in cerebral tissue were detected.RESULTS:Compared with control group,in captopril group the content of MDA decreased(P<0.05),the activity of SOD,GSH-Px hadn’t changed obviously.The activity of Ca2+-Mg2+-ATP enzyme and Na+-K+-ATP enzyme declined,but there was no statistical significance.CONCLUSION:Oral does of captopril for a long time can reduce free radicals and strengthen the antioxidant function of cerebral tissue,but it may damage the neuron membrane function of cerebral tissue.更多还原