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木犀草素通过减少 ROS 介导的氧化应激来减轻吡虫啉诱导的大鼠脑线粒体神经毒性。

Luteolin attenuates Fipronil-induced neurotoxicity through reduction of the ROS-mediated oxidative stress in rat brain mitochondria.

机构信息

Department of Occupational Health and Safety Engineering, School of Health, Alborz University of Medical Sciences, Karaj, Iran; Research Center for Health, Safety and Environment, Alborz University of Medical Sciences, Karaj, Iran.

Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

出版信息

Pestic Biochem Physiol. 2021 Mar;173:104785. doi: 10.1016/j.pestbp.2021.104785. Epub 2021 Jan 21.

DOI:10.1016/j.pestbp.2021.104785
PMID:33771263
Abstract

Luteolin (LUT) as a natural compound found in vegetables and fruits has various pharmacological effects. Fipronil (FPN), as a pesticide, has been considered for its effect on the antioxidant system and induction of oxidative stress. This study was designed to investigate the protective effects of LUT against the oxidative stress and mitochondrial toxicity induced by FPN on the rat brain. Several parameters such as mitochondrial reactive oxygen species (ROS) level, mitochondrial membrane potential (MMP) collapse, mitochondrial swelling, cytochrome c release, mitochondrial glutathione (GSH), lipid peroxidation (LPO) and Adenosine triphosphate (ATP) levels were assessed. Results indicated that the administration of LUT (25 μM) significantly improved oxidative stress and mitochondrial damages induced via FPN (6, 12 and 24 μM) in isolated mitochondria from the brain. These results show that LUT exerted protective effects against FPN-induced neurotoxicity in vitro through improving oxidative stress and mitochondrial damages.

摘要

木犀草素 (LUT) 作为一种存在于蔬菜和水果中的天然化合物,具有多种药理作用。氟虫腈 (FPN) 作为一种杀虫剂,因其对抗氧化系统的影响和诱导氧化应激而受到关注。本研究旨在探讨 LUT 对氟虫腈诱导的大鼠脑内氧化应激和线粒体毒性的保护作用。评估了几种参数,如线粒体活性氧 (ROS) 水平、线粒体膜电位 (MMP) 崩溃、线粒体肿胀、细胞色素 c 释放、线粒体谷胱甘肽 (GSH)、脂质过氧化 (LPO) 和三磷酸腺苷 (ATP) 水平。结果表明,LUT(25 μM)的给药可显著改善通过 FPN(6、12 和 24 μM)诱导的分离脑线粒体中的氧化应激和线粒体损伤。这些结果表明,LUT 通过改善氧化应激和线粒体损伤,在体外发挥对氟虫腈诱导的神经毒性的保护作用。

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