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本文引用的文献

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Inhibitory effect of α-tocopherol on methylmercury-induced oxidative steress.α-生育酚对甲基汞诱导的氧化应激的抑制作用。
Environ Health Prev Med. 2004 May;9(3):111-7. doi: 10.1007/BF02898069.
2
Bacopa monniera ameliorates amnesic effects of diazepam qualifying behavioral-molecular partitioning.假马齿苋可改善地西泮的失忆效应,符合行为-分子分区情况。
Neuroscience. 2008 Aug 13;155(2):476-84. doi: 10.1016/j.neuroscience.2008.05.043. Epub 2008 Jun 7.
3
Daily mercury intake in fish-eating populations in the Brazilian Amazon.巴西亚马逊地区食鱼人群的每日汞摄入量。
J Expo Sci Environ Epidemiol. 2008 Jan;18(1):76-87. doi: 10.1038/sj.jes.7500599. Epub 2007 Sep 5.
4
Role of docosahexaenoic acid in modulating methylmercury-induced neurotoxicity.二十二碳六烯酸在调节甲基汞诱导的神经毒性中的作用。
Toxicol Sci. 2007 Dec;100(2):423-32. doi: 10.1093/toxsci/kfm224. Epub 2007 Aug 29.
5
Cipura paludosa extract prevents methyl mercury-induced neurotoxicity in mice.沼泽刺蕊草提取物可预防甲基汞诱导的小鼠神经毒性。
Basic Clin Pharmacol Toxicol. 2007 Aug;101(2):127-31. doi: 10.1111/j.1742-7843.2007.00091.x.
6
Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity.谷氨酸和活性氧在甲基汞神经毒性中的作用。
Braz J Med Biol Res. 2007 Mar;40(3):285-91. doi: 10.1590/s0100-879x2007000300001.
7
Postnatal methylmercury exposure induces hyperlocomotor activity and cerebellar oxidative stress in mice: dependence on the neurodevelopmental period.出生后甲基汞暴露诱导小鼠运动活动亢进和小脑氧化应激:依赖于神经发育时期。
Neurochem Res. 2006 Apr;31(4):563-9. doi: 10.1007/s11064-006-9051-9. Epub 2006 May 9.
8
Cerebellar thiol status and motor deficit after lactational exposure to methylmercury.哺乳期暴露于甲基汞后小脑硫醇状态与运动功能障碍
Environ Res. 2006 Sep;102(1):22-8. doi: 10.1016/j.envres.2006.02.003. Epub 2006 Mar 29.
9
Herbal remedies for anxiety - a systematic review of controlled clinical trials.用于治疗焦虑症的草药疗法——对照临床试验的系统评价
Phytomedicine. 2006 Feb;13(3):205-8. doi: 10.1016/j.phymed.2004.11.006. Epub 2005 Aug 15.
10
Protective effects of Polygala paniculata extract against methylmercury-induced neurotoxicity in mice.瓜子金提取物对小鼠甲基汞诱导的神经毒性的保护作用。
J Pharm Pharmacol. 2005 Nov;57(11):1503-8. doi: 10.1211/jpp.57.11.0017.

印度蔊菜对甲基汞诱导的大鼠小脑氧化应激的保护作用。

Protective effect of Bacopa monniera on methyl mercury-induced oxidative stress in cerebellum of rats.

机构信息

Department of Medical Biochemistry, University of Madras, Taramani Campus, Chennai, Tamil Nadu, India.

出版信息

Cell Mol Neurobiol. 2012 Aug;32(6):979-87. doi: 10.1007/s10571-012-9813-7. Epub 2012 Feb 26.

DOI:10.1007/s10571-012-9813-7
PMID:22366895
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11498485/
Abstract

Methyl mercury (MeHg) is a ubiquitous environmental pollutant leading to neurological and developmental deficits in animals and human beings. Bacopa monniera (BM) is a perennial herb and is used as a nerve tonic in Ayurveda, a traditional medicine system in India. The objective of the present study was to investigate whether Bacopa monniera extract (BME) could potentially inhibit MeHg-induced toxicity in the cerebellum of rat brain. Male Wistar rats were administered with MeHg orally at a dose of 5 mg/kg b.w. for 21 days. Experimental rats were given MeHg and also administered with BME (40 mg/kg, orally) for 21 days. After the treatment period, we observed that MeHg exposure significantly inhibited the activities of superoxide dismutase, catalase, glutathione peroxidase, and increased the glutathione reductase activity in cerebellum. It was also found that the level of thiobarbituric acid-reactive substances was increased with the concomitant decrease in the glutathione level in MeHg-induced rats. These alterations were prevented by the administration of BME. Behavioral interference in the MeHg-exposed animals was evident through a marked deficit in the motor performance in the rotarod task, which was completely recovered to control the levels by BME administration. The total mercury content in the cerebellum of MeHg-induced rats was also increased which was measured by atomic absorption spectrometry. The levels of NO(2) (-) and NO(3) (-) in the serum were found to be significantly increased in the MeHg-induced rats, whereas treatment with BME significantly decreased their levels in serum to near normal when compared to MeHg-induced rats. These findings strongly implicate that BM has potential to protect brain from oxidative damage resulting from MeHg-induced neurotoxicity in rat.

摘要

甲基汞(MeHg)是一种普遍存在的环境污染物,可导致动物和人类的神经和发育缺陷。印度传统医学体系阿育吠陀中,将益智(Bacopa monniera)作为一种神经滋补品。本研究旨在探讨益智提取物(BME)是否可能抑制 MeHg 诱导的大鼠脑小脑毒性。雄性 Wistar 大鼠经口给予 MeHg 剂量为 5mg/kg bw,连续 21 天。实验组大鼠给予 MeHg 并同时给予 BME(40mg/kg,口服)连续 21 天。治疗期结束后,我们观察到 MeHg 暴露显著抑制了小脑中超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶的活性,同时增加了谷胱甘肽还原酶的活性。还发现 MeHg 诱导的大鼠中,硫代巴比妥酸反应物质的水平增加,同时谷胱甘肽水平降低。BME 的给予可预防这些改变。MeHg 暴露动物的行为干扰明显,表现在旋转棒任务中的运动表现明显缺陷,而 BME 的给予则完全恢复到对照水平。原子吸收光谱法测量 MeHg 诱导大鼠小脑中的总汞含量也增加。MeHg 诱导大鼠血清中 NO(2) (-) 和 NO(3) (-) 的水平显著升高,而 BME 的治疗则显著降低了它们的水平,使其接近正常水平。这些发现强烈表明,益智具有保护大脑免受 MeHg 诱导的神经毒性引起的氧化损伤的潜力。