Pinto Carmen, Cestero Juan J, Rodríguez-Galdón Beatriz, Macías Pedro
Department of Biochemistry and Molecular Biology, Science Faculty, Extremadura University, Av. Elvas s/n, 06006 Badajoz, Spain.
Toxicol Rep. 2014 Sep 16;1:726-733. doi: 10.1016/j.toxrep.2014.09.004. eCollection 2014.
Ethanol-mediated free radical generation is directly involved in alcoholic liver disease. In addition, chronic alcohol bingeing also induces pathological changes and dysfunction in multi-organs. In the present study, the protective effect of xanthohumol (XN) on ethanol-induced damage was evaluated by determining antioxidative parameters and stress oxidative markers in liver, kidney, lung, heart and brain of rats. An acute treatment (4 g/kg b.w.) of ethanol resulted in the depletion of superoxide dismutase, catalase and glutathione S-transferase activities and reduced glutathione content. This effect was accompanied by the increased activity of tissue damage marker enzymes (glutamate oxaloacetate transaminase, glutamate pyruvate transaminase and lactate dehydrogenase) and a significant increase in lipid peroxidation and hydrogen peroxide concentrations. Pre-treatment with XN protected rat tissues from ethanol-induced oxidative imbalance and partially mitigated the levels to nearly normal levels in all tissues checked. This effect was dose dependent, suggesting that XN reduces stress oxidative and protects rat tissues from alcohol-induced injury.
乙醇介导的自由基生成直接参与酒精性肝病的发生。此外,长期酗酒还会引起多器官的病理变化和功能障碍。在本研究中,通过测定大鼠肝脏、肾脏、肺、心脏和大脑中的抗氧化参数和氧化应激标志物,评估了黄腐酚(XN)对乙醇诱导损伤的保护作用。急性给予乙醇(4 g/kg体重)导致超氧化物歧化酶、过氧化氢酶和谷胱甘肽S-转移酶活性降低,谷胱甘肽含量减少。这种效应伴随着组织损伤标志物酶(谷氨酸草酰乙酸转氨酶、谷氨酸丙酮酸转氨酶和乳酸脱氢酶)活性增加以及脂质过氧化和过氧化氢浓度显著升高。XN预处理可保护大鼠组织免受乙醇诱导的氧化失衡影响,并使所有检测组织中的水平部分减轻至接近正常水平。这种效应具有剂量依赖性,表明XN可减轻氧化应激并保护大鼠组织免受酒精诱导的损伤。