Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Life Sci. 2018 Apr 1;198:38-45. doi: 10.1016/j.lfs.2018.02.022. Epub 2018 Feb 15.
Arsenic is a well-known environmental contaminant, causing toxicity in different organs. The aim of this study was to investigate the possible neuroprotective effect of ellagic acid (EA) on arsenic-induced neurotoxicity in rats.
Animals were divided into five groups. The first group received normal saline (2 mL/kg) for 21 days as control group. Group 2 was orally treated with sodium arsenite (SA, 10 mg/kg) for 21 days. Groups 3 and 4 were orally treated with SA (10 mg/kg) for 7 days prior to EA (10 and 30 mg/kg respectively) treatment and continued up to 21 days simultaneously with SA administration. Group 5 was orally treated with EA (30 mg/kg) for 14 days. Passive avoidance test and rotarod test were done to evaluate the behavioral changes following SA and/or EA treatment. Different biochemical, histological and molecular biomarkers were assessed in the brain tissue.
Our data showed that SA significantly elevated brain tissue arsenic levels and malondialdehyde, nitric oxide, protein carbonylation, tumor necrosis factor-alpha, and interlukein-1β production. A decrease in the total antioxidant capacity, reduced glutathione content and glutathione peroxidase activity occurred in the brain of rats exposed to SA. SA-treated rats showed a significant impairment in long-term-memory, motor coordination and equilibrium. These results were supported by histopathological observations of the brain. Results revealed that administration of EA (30 mg/kg) reversed all neural markers alternation and ameliorated behavioral and histopathological changes induced by SA.
EA can effectively protect brain tissue against SA-induced neurotoxicity via its antioxidant and anti-inflammatory effects.
砷是一种众所周知的环境污染物，会对不同器官造成毒性。本研究旨在探讨鞣花酸（EA）对大鼠砷诱导神经毒性的可能神经保护作用。
动物分为五组。第一组给予生理盐水（2mL/kg），作为对照组，共 21 天。第二组连续 21 天口服亚砷酸钠（SA，10mg/kg）。第三组和第四组在口服 SA（10mg/kg）7 天后开始同时给予 EA（10 和 30mg/kg）治疗，直至 21 天。第五组连续 14 天口服 EA（30mg/kg）。通过被动回避试验和转棒试验评估 SA 和/或 EA 处理后行为变化。评估脑组织中的不同生化、组织学和分子生物标志物。
我们的数据表明，SA 显著增加了脑组织中的砷含量以及丙二醛、一氧化氮、蛋白质羰基化、肿瘤坏死因子-α和白细胞介素-1β的产生。暴露于 SA 的大鼠脑组织中的总抗氧化能力、还原型谷胱甘肽含量和谷胱甘肽过氧化物酶活性下降。SA 处理的大鼠在长期记忆、运动协调和平衡方面表现出明显的损伤。这些结果得到了大脑组织病理学观察的支持。结果表明，EA（30mg/kg）的给药逆转了所有神经标志物的改变，并改善了 SA 引起的行为和组织病理学变化。
EA 通过其抗氧化和抗炎作用，可有效保护脑组织免受 SA 诱导的神经毒性。
