苯乙福明减轻长期服用乙醇大鼠肝脏的氧化-亚硝基应激反应

A. Mykytenko, O. Akimov, G. Yeroshenko, K. Neporada
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摘要

调节 AMP 激活蛋白激酶 (AMPK) 通路的活性被认为是开发慢性酒精性肝炎治疗方法的一个很有前景的选择。据报道,苯乙双胍(一种双胍类药物)可提高 AMPK 的活性。这项工作的目的是评估苯乙双胍作为 AMPK 激活剂对长期服用乙醇条件下大鼠肝脏氧化-亚硝基应激发展的影响。实验以 24 只雄性 Wistar 大鼠为对象,分为 4 组:对照组;连续 63 天每天口服 10 毫克/千克剂量盐酸苯乙福明的动物;通过腹腔注射 16.5%乙醇溶液(含 5%葡萄糖),以 4 毫升/千克体重的速度间歇性强迫酒精中毒 5 天,随后改用 10%乙醇作为唯一饮酒来源的动物;模拟慢性酒精性肝炎和服用苯乙福明的动物。对肝匀浆中的超氧化物歧化酶、过氧化氢酶、氮氧化物合成酶同工酶活性、超氧阴离子自由基产生量、丙二醛浓度、过亚硝酸盐、亚硝基硫醇浓度和蛋白质氧化修饰(OMP)进行了评估。结果发现,长期服用乙醇的大鼠肝脏中氧和氮活性形式的生成增加,OMP 加剧。结果表明,在长期服用乙醇的情况下引入苯乙福明可限制过氧化亚硝酸盐的过量形成,并防止大鼠肝脏蛋白质的氧化损伤。关键词AMP激活蛋白激酶 慢性酒精性肝炎 肝脏 氧化和亚硝酸应激 苯乙福明
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Phenformin attenuates the oxidative-nitrosative stress in the liver of rats under long-term ethanol administration
Modulation of the AMP-activated protein kinase (AMPK) pathway activity is considered to be a promi­sing option in the development of approaches to chronic alcoholic hepatitis treatment. Phenformin, which is a biguanide, has been reported to increase AMPK activity. The aim of this work was to estimate the effect of phenformin as AMPK activator on the development of oxidative-nitrosative stress in the liver of rats under conditions of long-term ethanol administration. The experiments were performed on 24 male Wistar rats, divided into 4 groups: control; animals, which received phenformin hydrochloride orally at a dose of 10 mg/kg daily for 63 days; animals with a forced intermittent alcoholization for 5 days by intraperitoneal administration of 16.5% ethanol solution in 5% glucose at the rate of 4 ml/kg b.w. and subsequent transfer to 10% ethanol as the only source of drinking; animals with chronic alcohol hepatitis simulation and phenformin administration. Superoxide dismutase, catalase, NO synthase isoforms activity, superoxide anion radical production, concentration of malonic dialdehyde, peroxynitrite, nitrites, nitrosothiols concentration and oxidative modification of proteins (OMP) were estimated in liver homogenates. The increased production of oxygen and nitrogen active forms and OMP intensification in the liver of rats under long-term administration of ethanol was detected. Phenformin introduction under long-term ethanol administration was shown to limit the excess peroxynitrite formation and to prevent oxidative damage to rat liver proteins. Keywords: AMP-activated protein kinase., chronic alcoholic hepatitis, liver, oxidative and nitrosative stress, phenformin
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