黑皮油对大鼠乙酰胆碱酯酶和氧化功能障碍导致的工作记忆受损有保护作用

Imam Aminu, Alakoso Jumoke Teslimat, W. Victoria, C. Samson, Oyewole Lukuman Aboyeji, O. Olatunbosun, Shittu Toyin Sheu-Tijani, Ajao Moyosore Saliu
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引用次数: 1

摘要

有机磷中毒的氧化损伤与神经认知缺陷有关。本研究探讨黑草油(NSO)减轻敌敌畏(DDVP)诱导的大鼠氧化损伤和神经认知功能障碍的保护作用。将32只大鼠随机分为4组,分别给予生理盐水1 ml/kg、DDVP 8.8 mg/kg、DDVP + NSO 1 ml/kg、NSO连续14 d。在实验第1天和第15天记录大鼠体重,在Morris水迷宫中分别于第11、12和13天进行3次实验,随后在第14天记录隐藏平台潜伏期和平台象限时间,作为长期记忆(LTM)、短期记忆(STM)和参考记忆的测量指标。第15天对大鼠实施安乐死,切除大鼠大脑,每组取5只大鼠海马,均质分析总活性氧(ROS)、氧化亚氮(NO)水平和乙酰胆碱酯酶(AChE)活性,其余3只进行组织学和Ki67免疫组织化学处理。DDVP暴露导致海马NO和ROS水平显著升高,AChE活性和Ki67蛋白表达降低。这与逃逸潜伏期延迟和平台象限时间缩短有关。NSO干预可抑制ROS和NO的爆发,保护神经源性细胞,改善神经认知指标。因此,我们得出结论,稳定氧化和神经原功能对保护免受DDVP海马损伤至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nigella sativa oil protected the hippocampus against Acetyl cholinesterase and oxidative dysfunctions-driven impaired working memory in rats
Oxidative damages in organophosphates poisoning is associated with neuro-cognitive deficits. This study investigates the protective effect of Nigella sativa oil (NSO) in mitigating dichlorvos (DDVP) induced oxidative damage and neuro-cognitive impairment in rats. Thirty-two rats were randomly divided into four groups, exposed to 1 ml/kg of normal saline, 8.8 mg/kg of DDVP, DDVP + 1 ml/kg of NSO and NSO respectively for 14 consecutive days. Body weights were recorded at day 1 and 15 of the experiment, the rats were exposed to 3 trials each on the 11, 12 and 13th days in the Morris water maze, and subsequently latency to hidden platform and time in the platform quadrant were recorded as measures of long term memory (LTM), short term memory (STM) and reference memory on the 14th day. The rats were euthanized on the 15th day, the brains excised and the hippocampi of five brains in each group were removed, homogenized to analyze for total reactive oxygen species (ROS), nitrous oxide (NO) levels and acetylcholinesterase (AChE) activities, while the other three were processed for histology and Ki67 immunohistochemistry. DDVP exposure caused a significant increase in hippocampal NO and ROS levels, with reductions in AChE activities and Ki67 protein expression. This was associated with delayed escape latency and reduced time in platform quadrant. NSO intervention prevented outburst in ROS and NO, preserved the neurogenic cells and improved neuro-cognitive indices. We thus conclude that stabilizing oxidative and neurogenic functions are vital to protect against DDVP hippocampal insults.
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