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百里醌和番茄红素的抗氧化及抗炎潜力减轻了毒死蜱诱导的中毒性神经病。

Antioxidant and Anti-Inflammatory Potential of Thymoquinone and Lycopene Mitigate the Chlorpyrifos-Induced Toxic Neuropathy.

作者信息

Aboubakr Mohamed, Elshafae Said M, Abdelhiee Ehab Y, Fadl Sabreen E, Soliman Ahmed, Abdelkader Afaf, Abdel-Daim Mohamed M, Bayoumi Khaled A, Baty Roua S, Elgendy Enas, Elalfy Amira, Baioumy Bodour, Ibrahim Samah F, Abdeen Ahmed

机构信息

Department of Pharmacology, Faculty of Veterinary Medicine, Benha University, Toukh 13736, Egypt.

Department of Pathology, Faculty of Veterinary Medicine, Benha University, Toukh 13736, Egypt.

出版信息

Pharmaceuticals (Basel). 2021 Sep 20;14(9):940. doi: 10.3390/ph14090940.

DOI:10.3390/ph14090940
PMID:34577640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8468258/
Abstract

CPF (chlorpyrifos) is an organophosphate pesticide used in agricultural and veterinary applications. Our experiment aimed to explore the effects of thymoquinone (TQ) and/or lycopene (LP) against CPF-induced neurotoxicity. Wistar rats were categorized into seven groups: first group served as a control (corn oil only); second group, TQ (10 mg/kg); third group, LP (10 mg/kg); fourth group, CPF (10 mg/kg) and deemed as CPF toxic control; fifth group, TQ + CPF; sixth group, (LP + CPF); and seventh group, (TQ + LP + CPF). CPF intoxication inhibited acetylcholinesterase (AchE), decreased glutathione (GSH) content, and increased levels of malondialdehyde (MDA), an oxidative stress biomarker. Furthermore, CPF impaired the activity of antioxidant enzymes including superoxide dismutase (SOD) and catalase (CAT) along with enhancement of the level of inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β. CPF evoked apoptosis in brain tissue. TQ or LP treatment of CPF-intoxicated rats greatly improved AchE activity, oxidative state, inflammatory responses, and cell death. Co-administration of TQ and LP showed better restoration than their sole treatment. In conclusion, TQ or LP supplementation may alleviate CPF-induced neuronal injury, most likely due to TQ or LPs' antioxidant, anti-inflammatory, and anti-apoptotic effects.

摘要

毒死蜱(CPF)是一种用于农业和兽医领域的有机磷农药。我们的实验旨在探究百里醌(TQ)和/或番茄红素(LP)对CPF诱导的神经毒性的影响。将Wistar大鼠分为七组:第一组作为对照组(仅给予玉米油);第二组,TQ(10毫克/千克);第三组,LP(10毫克/千克);第四组,CPF(10毫克/千克),视为CPF毒性对照组;第五组,TQ + CPF;第六组,(LP + CPF);第七组,(TQ + LP + CPF)。CPF中毒抑制了乙酰胆碱酯酶(AchE),降低了谷胱甘肽(GSH)含量,并增加了氧化应激生物标志物丙二醛(MDA)的水平。此外,CPF损害了包括超氧化物歧化酶(SOD)和过氧化氢酶(CAT)在内的抗氧化酶的活性,同时提高了炎症介质如肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-6和IL-1β的水平。CPF诱发了脑组织的细胞凋亡。用TQ或LP治疗CPF中毒的大鼠可显著改善AchE活性、氧化状态、炎症反应和细胞死亡。TQ和LP联合给药显示出比单独给药更好的恢复效果。总之,补充TQ或LP可能减轻CPF诱导的神经元损伤,这很可能是由于TQ或LP的抗氧化、抗炎和抗凋亡作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c67/8468258/f15fb9e92115/pharmaceuticals-14-00940-g007.jpg
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