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N-乙酰半胱氨酸对大鼠不同脑区久效磷诱导的氧化应激的神经保护作用。

Neuroprotective Effect of N-acetylcysteine Against Monocrotophos-Induced Oxidative Stress in Different Brain Regions of Rats.

机构信息

Department of Biochemistry, Maharshi Dayanand University, Rohtak, 124001, Haryana, India.

出版信息

Appl Biochem Biotechnol. 2022 Sep;194(9):4049-4065. doi: 10.1007/s12010-022-03967-9. Epub 2022 May 19.

Abstract

Monocrotophos (MCP) is systemic organophosphate insecticide used against crop pests. It is reported to cause mammalian toxicity through both acute and chronic exposure. In the present study, we have shown the protective role of N-acetylcysteine (NAC) against MCP-induced oxidative stress in frontal cortex, corpus striatum and hippocampus brain regions of rats. Male Albino Wistar rats were divided into control, NAC-treated, MCP and NAC + MCP-treated groups. An oral dose of MCP (0.9 mg/kg b.wt) and NAC (200 mg/kg b.wt) was administered for 28 days. Results showed an increase in lipid peroxidation (LPO) and protein oxidation followed by decreased antioxidant enzymes after 28 days of MCP exposure. Histopathological analysis showed that monocrotophos exposure caused neurodegenerative changes as evident by neurons with dystrophic changes in the form of shrunken hyperchromatic nuclei in all the regions of the rat brain. N-acetylcysteine supplementation to MCP-treated rats showed a reduction in oxidative stress and ameliorated cellular alterations in all of the three regions. The results of the study indicate that N-acetylcysteine offers neuroprotection by improving antioxidant response and decreasing oxidative stress in different regions of the rat brain.

摘要

久效磷(MCP)是一种用于防治农作物害虫的内吸性有机磷杀虫剂。据报道,它会通过急性和慢性暴露对哺乳动物造成毒性。在本研究中,我们已经证明了 N-乙酰半胱氨酸(NAC)对 MCP 诱导的大鼠额皮质、纹状体和海马脑区氧化应激的保护作用。雄性白化 Wistar 大鼠被分为对照组、NAC 处理组、MCP 处理组和 NAC+MCP 处理组。MCP(0.9mg/kg b.wt)和 NAC(200mg/kg b.wt)的口服剂量连续给药 28 天。结果显示,MCP 暴露 28 天后,脂质过氧化(LPO)和蛋白质氧化增加,随后抗氧化酶减少。组织病理学分析显示,久效磷暴露导致神经退行性改变,所有大鼠脑区的神经元均出现皱缩、深染核的退行性改变。MCP 处理大鼠补充 N-乙酰半胱氨酸后,所有三个区域的氧化应激均减少,细胞改变得到改善。研究结果表明,N-乙酰半胱氨酸通过提高抗氧化反应和降低大鼠脑不同区域的氧化应激来提供神经保护作用。

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