姜黄素抗戊四唑致癫痫大鼠氧化损伤的抗氧化潜力。

V Sharma, B Nehru, A Munshi, A Jyothy
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引用次数: 49

摘要

Pentylenetetrazol (PTZ)诱导的氧化应激导致大鼠抗氧化酶状态紊乱,并伴有神经元损伤和癫痫的发生。本研究评估了姜黄素对ptz诱发的惊厥的抗氧化作用。在30天的时间里,隔天腹腔注射亚惊厥剂量的PTZ导致了众所周知的癫痫点燃模型的发展。分光光度分析显示,ptz诱导的氧化应激可显著提高癫痫大鼠大脑和小脑中抗氧化酶丙二醛(MDA)、过氧化氢酶和谷胱甘肽s -转移酶(GST)的活性。以2 g/kg的剂量口服姜黄素30天,可导致大鼠大脑和小脑中MDA、过氧化氢酶和GST水平的短暂降低。胡椒碱(20mg /kg口服)与姜黄素一起服用,姜黄素的生物利用度提高了20倍以上。姜黄素与卡马西平联合治疗(口服3.6 mg/kg)也得到了类似的结果,表明姜黄素具有强抗氧化作用,可作为抗癫痫治疗的辅助药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Antioxidant potential of curcumin against oxidative insult induced by pentylenetetrazol in epileptic rats.

Pentylenetetrazol (PTZ)-induced oxidative stress results in disturbance of the antioxidant enzyme status accompanied by neuronal injury and the development of epilepsy in rats. The present study evaluated the antioxidant effects of curcumin against PTZ-induced convulsions. Over a period of 30 days, i.p. injections of subconvulsive doses of PTZ on alternate days resulted in the development of a well-known kindling model of epilepsy. Spectrophotometric analysis revealed a markedly elevated activity of the antioxidant enzymes malondialdehyde (MDA), catalase and glutathione S-transferase (GST) in the cerebrum and cerebellum of epileptic rats due to PTZ-induced oxidative stress. Oral supplementation of curcumin at a dose of 2 g/kg for 30 days resulted in a transient decrease in MDA, catalase and GST levels in the rat cerebrum and cerebellum. Piperine (20 mg/kg orally) was administered along with curcumin to enhance the bioavailability of the latter up to 20-fold more. Combined treatment with curcumin and carbamazepine (3.6 mg/kg orally) also gave similar results, indicating that the potent antioxidant curcumin can be used as an adjuvant in antiepileptic therapy.

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