Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalai Nagar – 608002, Tamil Nadu, India.
Eur J Pharmacol. 2011 Jan 10;650(1):364-70. doi: 10.1016/j.ejphar.2010.09.068. Epub 2010 Oct 13.
Aim of the present study was planned to determine the protective role of naringin in attenuating the toxicity induced by nickel sulfate in rat liver. In this investigation nickel sulfate (20mg/kg body weight) was administered intraperitoneally for 20days to induce toxicity. Naringin was administered orally (20, 40 and 80mg/kg body weight) for 20days with intraperitoneal administration of nickel sulfate. Liver injury was measured by the increased activities of serum hepatic enzymes namely aspartate transaminase, alanine transaminase, alkaline phosphatase, gamma glutamyl transferase, lactate dehydrogenase and total bilirubin along with increased elevation of lipid peroxidation markers, thiobarbituric reactive acid substances, lipid hydroperoxides, protein carbonyl content and conjugated dienes. The toxic effect of nickel was also indicated by significantly decreased activities of enzymatic antioxidants like superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and glucose-6-phosphate dehydrogenase and non-enzymatic antioxidants like reduced glutathione, total sulfhydryl groups, vitamin C and vitamin E levels were significantly decreased. Naringin administered at a dose of 80mg/kg body weight significantly reversed the activities of hepatic marker enzymes, decreasing lipid peroxidative markers, increasing the antioxidant cascade and decreasing the nickel concentration in the liver. The effect at a dose of 80mg/kg body weight was more pronounced than that of other two doses (20 and 40mg/kg body weight). All these changes were supported by histopathological observations. These results clearly demonstrate that naringin has the potential in alleviating the toxic effects of nickel in rat liver.
本研究旨在确定柚皮苷在减轻硫酸镍诱导的大鼠肝毒性中的保护作用。在这项研究中，硫酸镍（20mg/kg 体重）腹腔内给药 20 天以诱导毒性。柚皮苷（20、40 和 80mg/kg 体重）经口给药，同时腹腔内给予硫酸镍。通过血清肝酶（天冬氨酸转氨酶、丙氨酸转氨酶、碱性磷酸酶、γ-谷氨酰转移酶、乳酸脱氢酶和总胆红素）活性的升高来衡量肝损伤，以及脂质过氧化标志物、硫代巴比妥酸反应性酸物质、脂质过氧化物、蛋白质羰基含量和共轭二烯的升高来衡量肝损伤。镍的毒性作用还表现为抗氧化酶如超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽-S-转移酶、谷胱甘肽还原酶和葡萄糖-6-磷酸脱氢酶的活性显著降低，非酶抗氧化剂如还原型谷胱甘肽、总巯基、维生素 C 和维生素 E 水平显著降低。柚皮苷以 80mg/kg 体重的剂量给药可显著逆转肝标志物酶的活性，降低脂质过氧化标志物，增加抗氧化剂级联反应，降低肝脏中的镍浓度。该剂量（80mg/kg 体重）的效果比其他两个剂量（20 和 40mg/kg 体重）更为明显。所有这些变化都得到了组织病理学观察的支持。这些结果清楚地表明，柚皮苷具有减轻大鼠肝镍毒性的潜力。
