橙皮苷保护肝细胞免受丙戊酸诱导的大鼠肝功能障碍

Mangaiah Suresh, S. Narashiman Kishore Kumar, Srinivasan Ashok Kumar, Krishnan Thulasi Raman, Murugaiyan Uma, Periandavan Kalaiselvi
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引用次数: 6

摘要

橙皮苷(HDN)是一种多酚类黄酮,因其清除自由基和抗氧化活性而受到广泛关注。丙戊酸钠(VPA)是常规使用的抗癫痫药物之一,也与肝毒性及其代谢物有关,如4-烯VPA和2,4-二烯。VPA是引起肝损伤的主要化合物。由于建议终生服用丙戊酸盐,通过服用安全的抗氧化剂来改善其毒性可能有利于保护肝脏。本实验旨在研究橙皮苷对丙戊酸钠肝毒性的拮抗作用。雄性Sprague-Dawley大鼠随机分为对照组、VPA组、HDN + VPA组和HDN组。口服VPA (300 mg/kg体重/天)和HDN (100 mg/kg体重/天)60天。实验结束时,处死大鼠,切除肝脏进行生化、mRNA和蛋白分析。采用肝标志物酶、氧化应激因子、抗氧化酶、凋亡蛋白mRNA和蛋白表达等指标评价大鼠肝毒性程度。通过对丙戊酸处理大鼠肝细胞的保护作用和防止肝细胞凋亡的能力来评价橙皮苷的功效。丙戊酸处理大鼠肝脏标志物酶活性、大分子损伤及促凋亡和抗凋亡蛋白基因表达均发生改变,而橙皮苷共处理大鼠则表现出明显的保护作用。橙皮苷通过抑制脂质过氧化和防止细胞进入凋亡,保护肝脏免受丙戊酸诱导的毒性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hesperidin safeguards hepatocytes from valproate-induced liver dysfunction in Sprague-Dawley rats

Hesperidin (HDN), a polyphenolic flavonoid, had drawn attention due to its free radical scavenging and antioxidant activity. Valproate (VPA) is one of the routinely used antiepileptic drugs that has also been associated with hepatotoxicity and its metabolites, like 4-ene VPA and 2,4-diene. VPA are the main contributory compounds in inducing hepatic damage. As lifelong intake of valproate has been recommended, ameliorating its toxicity by administration of safe antioxidants might be beneficial in protecting the liver. The current experiment was designed to test the efficacy of hesperidin on counteracting valproate-induced hepatotoxicity. Male Sprague-Dawley rats were randomly assigned into four groups: Control, VPA, HDN + VPA and HDN. VPA (300 mg/kg bwt/day) and HDN (100 mg/kg bwt/day) were administered orally for 60 days. At the end of the experimental period, rats were sacrificed and liver was excised for biochemical, mRNA and protein analysis. The extent of hepatotoxicity was assessed by liver marker enzymes, oxidative stressors, antioxidant enzymes, mRNA and protein expression of apoptotic proteins. The efficacy of hesperidin was assessed by the ability to safeguard the liver and prevent apoptosis of the hepatocytes in valproate-treated rats. The activities of liver marker enzymes, macromolecular damage and gene expression of pro- and anti-apoptotic proteins were altered in valproate-treated rats when compared to control rats whereas hesperidin co-treated rats showed significant protection. Hesperidin protects the liver from valproate-induced toxicity by curtailing lipid peroxidation and preventing the cells from entering into apoptosis.

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