Mani Vijay, Arivalagan Sivaranjani, Siddique Aktarul Islam, Namasivayam Nalini
Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar, 608 002, Tamilnadu, India.
Mol Cell Biochem. 2016 Oct;421(1-2):169-81. doi: 10.1007/s11010-016-2798-7. Epub 2016 Aug 20.
Alcoholic liver disease is a direct result of alcohol-induced hepatotoxicity coupled with impaired hepatic regenerative activity. Our aim of the study was to investigate the beneficial effect of zingerone on hepatic oxidative stress and inflammation induced by ethanol in experimental rats. Male albino Wistar rats were divided into four groups. Rats of groups 1 and 2 received isocaloric glucose and dimethyl sulfoxide (2 % DMSO). Hepatotoxicity was induced in groups 3 and 4 by supplementing 30 % ethanol post orally for 60 days. Rats of groups 2 and 4 received zingerone (20 mg/kg body weight in 2 % DMSO p.o) daily during the final 30 days of the experimental period. Ethanol alone administered rats showed significant increase in the plasma and tissue lipid peroxidation markers such as thiobarbituric acid reactive substances, lipid hydroperoxides, conjugated dienes, and a significant decrease in the activities of plasma and tissue enzymic and non-enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, reduced glutathione, vitamin C, and vitamin E. Moreover, the presence of mast cells and increase in the expressions of inflammatory markers such as NF-κB, COX-2, TNF-α, and IL-6 and decrease in the expression of Nrf2 in the liver was observed in ethanol-fed rats. Supplementation with zingerone to ethanol-fed rats reversed the changes induced by ethanol in the experimental rats. Thus, zingerone, through its antioxidant and anti-inflammatory effects, may represent a therapeutic option to protect against ethanol-induced hepatotoxicity.
酒精性肝病是酒精诱导的肝毒性以及肝脏再生活性受损的直接结果。我们这项研究的目的是调查姜辣素对实验大鼠乙醇诱导的肝脏氧化应激和炎症的有益作用。雄性白化Wistar大鼠被分为四组。第1组和第2组大鼠接受等热量的葡萄糖和二甲基亚砜(2% DMSO)。第3组和第4组通过口服补充30%乙醇60天来诱导肝毒性。在实验期的最后30天,第2组和第4组大鼠每天接受姜辣素(20毫克/千克体重,溶于2% DMSO,口服)。单独给予乙醇的大鼠血浆和组织脂质过氧化标志物如硫代巴比妥酸反应性物质、脂质氢过氧化物、共轭二烯显著增加,血浆和组织酶性和非酶性抗氧化剂如超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽还原酶、还原型谷胱甘肽、维生素C和维生素E的活性显著降低。此外,在喂食乙醇的大鼠中观察到肝脏中肥大细胞的存在以及炎症标志物如NF-κB、COX-2、TNF-α和IL-6的表达增加以及Nrf2的表达减少。给喂食乙醇的大鼠补充姜辣素可逆转乙醇在实验大鼠中诱导的变化。因此,姜辣素通过其抗氧化和抗炎作用,可能是一种预防乙醇诱导的肝毒性的治疗选择。