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纳米硒可改善拟除虫菊酯诱导的神经毒性大鼠的氧化应激和炎症反应。

Nano selenium ameliorates oxidative stress and inflammatory response associated with cypermethrin-induced neurotoxicity in rats.

机构信息

Ministry of health, Tobruk, Libya.

Department of Pharmacology & Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia, Egypt.

出版信息

Ecotoxicol Environ Saf. 2020 Jun 1;195:110479. doi: 10.1016/j.ecoenv.2020.110479. Epub 2020 Apr 1.

DOI:10.1016/j.ecoenv.2020.110479
PMID:32199213
Abstract

Cypermethrin (CYP), a class II synthetic pyrethroid, is used to control household insects. CYP can cross the blood-brain barrier to exert neurotoxicity through changes in sodium ion channels. Selenium is an essential component of glutathione peroxidise enzyme; in addition, it shows a potential anti-inflammatory property. The present study aimed to investigate the neuroprotective role of Nano-Se on CYP-induced neurotoxicity. Twenty-four adult male Wister rats were randomly divided into three groups: a) control, b) CYP (1mg/kg) administered orally for 21 days, c) CYP (1mg/kg) administered orally for 21 days and Nano-Se (2.5 mg/kg) given once a day three times a week for three weeks). Locomotor activity was assessed using open field test then rats were sacrificed under anaesthesia, and their brains were dissected out and processed for biochemical and histopathological studies. Histological examination of CYP-treated rats demonstrated some degenerative changes; besides, CYP affected rat locomotor activity. CYP-treated rats showed increased levels of malondialdehyde (MDA), TNF-α and IL-1β in addition to the reduction of glutathione (GSH) levels and gamma-Aminobutyric acid (GABA). Nano-Se restored normal behavioural function and significantly attenuated CYP-evoked degenerative changes. Nano-Se increased levels of GABA and glutathione; on the other hand, it significantly prevented the rise in the levels of MDA, TNF-α and IL-1β. Therefore, Nano-Se demonstrated both anti-oxidant and anti-inflammatory potential. Nano-Se may be suggested to be a prospective candidate to ameliorate CYP-induced neurotoxicity.

摘要

氯菊酯(CYP)是一种二类合成拟除虫菊酯,用于控制家庭昆虫。CYP 可以穿过血脑屏障,通过改变钠离子通道发挥神经毒性作用。硒是谷胱甘肽过氧化物酶的必需成分;此外,它具有潜在的抗炎特性。本研究旨在探讨纳米硒对 CYP 诱导的神经毒性的神经保护作用。24 只成年雄性 Wister 大鼠随机分为三组:a)对照组,b)CYP(1mg/kg)口服 21 天,c)CYP(1mg/kg)口服 21 天,纳米硒(2.5mg/kg)每周 3 次,每天 1 次,连续 3 周)。通过旷场试验评估运动活动,然后在麻醉下处死大鼠,取出大脑进行生化和组织病理学研究。CYP 处理大鼠的组织学检查显示出一些退行性变化;此外,CYP 影响大鼠的运动活动。CYP 处理大鼠的丙二醛(MDA)、TNF-α 和 IL-1β 水平升高,谷胱甘肽(GSH)水平和γ-氨基丁酸(GABA)降低。纳米硒恢复了正常的行为功能,并显著减轻了 CYP 诱发的退行性变化。纳米硒增加了 GABA 和谷胱甘肽的水平;另一方面,它显著阻止了 MDA、TNF-α 和 IL-1β 水平的升高。因此,纳米硒表现出抗氧化和抗炎潜力。纳米硒可能被建议作为一种有前途的候选药物来改善 CYP 诱导的神经毒性。

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