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瑞香素对百草枯诱导的小鼠肝毒性的保护作用。

Protective role of thymoquinone against paraquat-induced hepatotoxicity in mice.

机构信息

Toxicology and Poisoning Research Centre, Tehran University of Medical Sciences, Tehran, Iran; Drug Design and Development Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Department of Pharmacology and Toxicology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran.

出版信息

Pestic Biochem Physiol. 2018 Jun;148:16-21. doi: 10.1016/j.pestbp.2018.03.006. Epub 2018 Mar 13.

DOI:10.1016/j.pestbp.2018.03.006
PMID:29891368
Abstract

Paraquat is a common and effective herbicide; although its poisoning could lead to severe oxidative organ damages and its main target organs are the lungs, kidneys, heart, and liver. Thymoquinone is the active ingredient of Nigella sativa which is traditionally used in herbal medicine; recent studies have shown that thymoquinone could inhibit oxidative stress. This study explores protective effects of thymoquinone on paraquat-induced hepatotoxicity in mice. Accordingly, adult male mice were randomly divided into nine groups for three continuous days intraperitoneal injection treatment: (1) control; (2) solvent; (3) 20 mg/kg vitamin E; (4) 20 mg/kg thymoquinone; (5) 20 mg/kg paraquat and Groups 6, 7, 8, and 9 received 20 mg/kg of vitamin E and 5, 10, and 20 mg/kg of thymoquinone, respectively. The last four groups, received 20 mg/kg paraquat just 24 h after pretreatments. We assessed serum liver enzymes activities, liver histopathology changes, oxidative (lipid peroxidation) and antioxidative (ferric reducing antioxidant power) potential, superoxide dismutase (SOD) and catalase activity, and total thiol groups content after administration of the poison and treatments. Pretreatment with 10 mg/kg thymoquinone inhibited, safely, the elevations in levels of liver function tests (LFTs) and lipid peroxidation, restored the activity of SOD, and ameliorated the histopathological alterations induced by paraquat. Eventually, our results indicate that thymoquinone performs its hepatoprotective role in mice by prevention of SOD suppression mediated by paraquat.

摘要

百草枯是一种常见且有效的除草剂;尽管其毒性可导致严重的氧化器官损伤,且其主要靶器官为肺、肾、心和肝。百里醌是黑种草中具有活性的成分,传统上被用于草药医学;最近的研究表明,百里醌可以抑制氧化应激。本研究旨在探讨百里醌对百草枯诱导的小鼠肝毒性的保护作用。因此,成年雄性小鼠被随机分为九组,连续三天进行腹腔注射治疗:(1)对照组;(2)溶剂组;(3)20mg/kg 维生素 E 组;(4)20mg/kg 百里醌组;(5)20mg/kg 百草枯组;以及 6、7、8、9 组分别接受 20mg/kg 维生素 E 和 5、10、20mg/kg 百里醌。后四组在预处理 24 小时后接受 20mg/kg 百草枯。我们在给药和治疗后评估了血清肝酶活性、肝组织病理学变化、氧化(脂质过氧化)和抗氧化(铁还原抗氧化能力)潜能、超氧化物歧化酶(SOD)和过氧化氢酶活性以及总硫醇含量。10mg/kg 百里醌预处理安全地抑制了肝功能试验(LFTs)和脂质过氧化水平的升高,恢复了 SOD 的活性,并改善了百草枯引起的组织病理学改变。最终,我们的结果表明,百里醌通过预防百草枯介导的 SOD 抑制,在小鼠中发挥其肝脏保护作用。

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