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姜黄素可保护小鼠大脑免受1-甲基-4-苯基-1,2,3,6-四氢吡啶引起的氧化应激。

Curcumin protects mouse brain from oxidative stress caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

作者信息

Rajeswari A

机构信息

Research School Department of Zoology, Annamalai University, Annamalai Nagar, Chidambaram, South India.

出版信息

Eur Rev Med Pharmacol Sci. 2006 Jul-Aug;10(4):157-61.

PMID:16910344
Abstract

We tested the hypothesis that curcumin, a polyphenolic antioxidant, acts as a powerful free radical scavenger in vivo in the brain, and interferes with oxidative stress caused by the parkinsonian neurotoxin, (MPTP) 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. We measured the (GSH) reduced glutathione levels, (TBARS) glutathione lipid peroxidation, (CAT) catalase and (SOD) superoxide dismutase activity in the (ST) striatum and (MB) mid brain 3rd day and 7th day following MPTP and curcumin administration. MPTP treatment caused a significant depletion in GSH and increased the specific activity of SOD, CAT and lipid peroxidation in both ST and MB on the 3rd and 7th day. MPTP induced GSH depletion and lipid peroxidation in ST and MB was blocked by curcumin treatment. Curcumin exhibited a synergistic effect on SOD and CAT activities in the ST and MB regions. The present study provides direct evidence for the involvement of curcumin in neuroprotection against oxidative stress.

摘要

我们验证了以下假说

姜黄素,一种多酚类抗氧化剂,在体内大脑中作为一种强大的自由基清除剂,并干扰由帕金森神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)引起的氧化应激。我们在给予MPTP和姜黄素后的第3天和第7天,测量了纹状体(ST)和中脑(MB)中还原型谷胱甘肽(GSH)水平、谷胱甘肽脂质过氧化产物(TBARS)、过氧化氢酶(CAT)和超氧化物歧化酶(SOD)活性。MPTP处理导致GSH显著耗竭,并在第3天和第7天增加了ST和MB中SOD、CAT的比活性以及脂质过氧化水平。姜黄素处理可阻断MPTP诱导的ST和MB中GSH耗竭及脂质过氧化。姜黄素对ST和MB区域的SOD和CAT活性具有协同作用。本研究为姜黄素参与对抗氧化应激的神经保护作用提供了直接证据。

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