Oxidative stress in the brain of nicotine-induced toxicity: protective role of Andrographis paniculata Nees and vitamin E
Oxidative stress in the brain of nicotine-induced toxicity: protective role of Andrographis paniculata Nees and vitamin E
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DOI：
10.1139/h08-147
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发表时间：
2009-04-01
影响因子：
3.4
通讯作者：
Roy, Somenath
中科院分区：
文献类型：
--
作者：
Das, Subhasis;Gautam, N.;Roy, Somenath
线粒体是几个关键细胞活动的十字路口；它们会产生大量的超氧自由基和过氧化氢，这些物质会破坏重要的大分子。尼古丁影响多种细胞过程，从诱导基因表达到调节酶活性。本研究旨在探讨穿心莲内酯（ANDRO）水提物（AE-Ap）和维生素E对尼古丁诱导大鼠脑线粒体的保护作用。在本研究中，尼古丁(1 mg（.)kg体质量（-1）天（-1））与2种香薷产品，ANDRO和AE-Ap (250 mg（.)kg体质量（-1）天（-1））同时处理，为期7天；各组雄性Wistar大鼠补充维生素E (50 mg（.)kg体重（-1）day(-1)）。在大脑的离散区域（大脑半球、小脑、间脑和脑干）测量线粒体电子传递链（Mito-ETC）复合物（I、II、III）、一氧化氮生成、超氧阴离子、过氧化氢酶、谷胱甘肽还原酶、谷胱甘肽过氧化物酶、谷胱甘肽- s转移酶的活性以及还原性谷胱甘肽和氧化性谷胱甘肽的浓度。研究发现，尼古丁抑制Mito- ETC复合物并产生一氧化氮，从而抑制脑不同区域线粒体氧化应激清除系统。在这些情况下，脂质过氧化和蛋白质氧化在脑线粒体的不同离散区域被注意到。ANDRO、AE-Ap和维生素E对尼古丁毒性具有保护作用。对这些变化的分析对于确定与尼古丁毒性相关的大脑正常功能障碍的基础是重要的，这些功能障碍可以通过金针叶和维生素E改善，并可能有助于开发针对尼古丁引起的疾病的治疗方法。
Mitochondria are the crossroads of several crucial cellular activities; they produce considerable quantities of superoxide radical and hydrogen peroxide, which can damage important macromolecules. Nicotine affects a variety of cellular processes, from induction of gene expression to modulation of enzymatic activities. The aim of this study was to elucidate the protective effects of andrographolide (ANDRO) aqueous extract (AE-Ap) of Andrographis paniculata, and vitamin E on nicotine-induced brain mitochondria. In this investigation, nicotine (1 mg(.)kg body mass(-1.)day(-1)) was treated, for the period of 7 days, simultaneously with 2 A. paniculata products, ANDRO and AE-Ap (250 mg(.)kg body mass(-1.)day(-1)); and vitamin E (50 mg(.)kg body mass(-1.)day(-1)) was supplemented in different group of male Wistar rats. The activities of mitochondrial electron transport chain (Mito-ETC) complexes (I, II, III), nitric oxide production, superoxide anion, catalase, glutathione reductase, glutathione peroxidase, glutathione-S-transferase, and concentrations of reduced glutathione and oxidized glutathione were measured in discrete regions of brain (the cerebral hemisphere, cerebellum, diencephalons, and brain stem). The study revealed that nicotine inhibits the Mito- ETC complexes and produces nitric oxide, which suppressed the mitochondrial oxidative stress scavenger system in different brain regions. In these circumstances, lipid peroxidation and protein oxidation were noted in different discrete regions of brain mitochondria. ANDRO, AE-Ap, and vitamin E showed the protective potentiality against nicotine toxicity. The analysis of such alterations is important in determining the basis of normal dysfunction in the brain associated with nicotine toxicity, which could be ameliorated by A. paniculata and vitamin E, and may help to develop therapeutic means against nicotine-induced disorders.