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芝麻油烟酸乙酯对 6-羟多巴胺诱导的小鼠神经毒性的神经保护作用:细胞、生化和神经化学证据。

Neuroprotective effect of sesame seed oil in 6-hydroxydopamine induced neurotoxicity in mice model: cellular, biochemical and neurochemical evidence.

机构信息

Department of Biotechnology, Jamia Hamdard-Hamdard University, New Delhi 110062, India.

出版信息

Neurochem Res. 2012 Mar;37(3):516-26. doi: 10.1007/s11064-011-0638-4. Epub 2011 Nov 17.

DOI:10.1007/s11064-011-0638-4
PMID:22089932
Abstract

Natural antioxidants have shown a remarkable reduction in oxidative stress due to excess formation of reactive oxygen species by enhancing antioxidant mechanism in the neurodegenerative disorders. Sesame seed oil (SO) is one of the most important edible oil in India as well as in Asian countries and has potent antioxidant properties thus the present study evaluated the neuroprotective effect of SO by using 6-Hydroxydopamine (6-OHDA)-induced Parkinson's disease model in mice. The mice were fed an SO mix diet for 15 days and then 6-OHDA was injected into the right striatum of mice brain. Three weeks after 6-OHDA infusion, mice were sacrificed and the striatum was removed. The neuroprotective role of SO on the activities of antioxidant and non-antioxidant enzymes such as glutathione reductase (GR), glutathione-S-transferase (GST), glutathione peroxidase (GPx), catalase (CAT) and content of glutathione (GSH) and thiobarbituric acid reactive substance (TBARS) were studied in the striatum. The activities of all the above-mentioned enzymes decreased significantly in 6-OHDA group (Lesioned) when compared with Sham. The pretreatment of SO on antioxidant mechanism and dopamine level in the brain had shown some significant improvement in Lesion+SO (L+SO) group when compared with Lesioned group. However, NADPH oxidase subunit, Nox2 and inflammatory stimulator Cox2 expression was increased as well as antioxidant MnSOD level was decreased in Lesioned group while SO showed the inhibitory effect on the activation of Nox2 and Cox2 and restored MnSOD expression in L+SO group. Increased tyrosine hydroxylase (TH) expression in substantia nigra as well as dopamine and its metabolite DOPAC level in L+SO group also support our findings that SO may inhibit activation of NADPH oxidase dependent inflammatory mechanism due to 6-OHDA induced neurotoxicity in mice.

摘要

天然抗氧化剂通过增强神经退行性疾病中的抗氧化机制,显示出对由于活性氧物种过度形成引起的氧化应激的显著降低。芝麻油(SO)是印度以及亚洲国家最重要的食用油之一,具有很强的抗氧化特性,因此本研究通过使用 6-羟多巴胺(6-OHDA)诱导的帕金森病模型来评估 SO 的神经保护作用。将 SO 混合饲料喂给小鼠 15 天,然后将 6-OHDA 注射到小鼠大脑的右侧纹状体中。6-OHDA 注射后 3 周,处死小鼠并取出纹状体。研究了 SO 对纹状体中抗氧化和非抗氧化酶(如谷胱甘肽还原酶(GR)、谷胱甘肽-S-转移酶(GST)、谷胱甘肽过氧化物酶(GPx)、过氧化氢酶(CAT)和谷胱甘肽(GSH)含量和硫代巴比妥酸反应物质(TBARS))的活性的神经保护作用。与 Sham 组相比,6-OHDA 组(损伤组)的所有上述酶的活性均明显降低。与损伤组相比,SO 预处理对大脑中的抗氧化机制和多巴胺水平的作用在损伤+SO(L+SO)组中显示出一些显著改善。然而,NADPH 氧化酶亚基、Nox2 和炎症刺激因子 Cox2 的表达增加,抗氧化 MnSOD 水平降低,而 SO 显示出抑制 Nox2 和 Cox2 激活的作用,并在 L+SO 组中恢复 MnSOD 表达。L+SO 组中黑质中酪氨酸羟化酶(TH)表达增加以及多巴胺及其代谢产物 DOPAC 水平升高也支持我们的发现,即 SO 可能通过抑制 NADPH 氧化酶依赖性炎症机制的激活来抑制 6-OHDA 诱导的小鼠神经毒性。

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