含粘液成分的饮食改善锰诱导的大鼠脑行为缺陷和组织学改变

Olayi Ogamode, Micheal Obu, O. Ijomone
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摘要

过度暴露于锰(Mn)已明确确定可引发神经毒性,可能导致帕金森样症状。据报道,麝香草含有可能具有神经保护作用的成分。本研究评估了pruriens构成的饮食对mn诱导的记忆和运动障碍的影响,以及对大脑组织学变化的影响。24只成年Wistar大鼠随机分为4组,每组6只。三组动物分别给予锰和标准饲料,饲料中含有10%或20%的褐毛鼠,持续5周。其余组为对照组,仅饲喂标准饲料。实验处理后,大鼠进行y形迷宫实验和空地实验。此外,脑切除和评估常规血红素和伊红组织学方案。自发交替y迷宫测试结果显示,Mn引起记忆能力下降,运动和探索活动减少,但与M. pruriens共同治疗可减轻行为障碍。此外,施用锰导致小脑、海马和纹状体出现明显的神经退行性特征。然而,同时使用金黄色分枝杆菌的饮食稍微减弱了组织学改变。综上所述,本研究表明,瘙痒分枝杆菌治疗可能对mn诱导的神经毒性有改善作用
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mucuna pruriens Constituted Diet Ameliorates Manganese-Induced Behavioural Deficit and Histological Alterations in the Brains of Rats
Overexposure to manganese (Mn) has been clearly established to trigger neurotoxicity that may result in Parkinson-like symptoms. Mucuna pruriens have been reported to possess constituents that could be neuroprotective. The present study evaluated the effect of M. pruriens constituted diet in Mn-induced memory and motor deficits, as well as on histological changes in the brain. Twenty-four adult Wistar rats were randomly assigned into four groups of six rats. Three groups of animals were subjected to Mn-administration and on standard feed, 10% or 20% M. pruriens constituted feeds for a 5-week duration. The remaining group served as control and received standard feed only. Following experimental treatments, rats were subjected to the Y-maze test and the open-field test. Furthermore, brains were excised and evaluated with routine haematoxylin and eosin histological protocol. Result of spontaneous alternation in the Y-maze test showed that Mn caused decreased memory performance and decreasing motor and explorative activities, but co-treatment with M. pruriens mitigated behavioural impairments. Additionally, Mn-administration resulted in noticeable neurodegenerative features in the cerebellum, hippocampus and striatum. However, concurrent use of M. pruriens diet slightly attenuated histological alterations. In conclusion, the present study suggests that treatment with M. pruriens may provide ameliorative benefits against Mn-induced neurotoxicity
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