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阿司匹林通过线粒体机制对百草枯诱导的肺毒性的改善作用。

Ameliorative role of aspirin in paraquat-induced lung toxicity via mitochondrial mechanisms.

机构信息

Forensic Medicine and Clinical Toxicology, Shiraz University of Medical Sciences, Shiraz, Iran.

Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran.

出版信息

J Biochem Mol Toxicol. 2019 Sep;33(9):e22370. doi: 10.1002/jbt.22370. Epub 2019 Jul 26.

DOI:10.1002/jbt.22370
PMID:31348582
Abstract

Paraquat (PQ) has accounted for numerous suicide attempts in developing countries. Aspirin (ASA) as an adjuvant treatment in PQ poisoning has an ameliorative role. And, it's uncoupling of mitochondrial oxidative phosphorylation role has been well established. The current study aimed at examining the aspirin mechanism on lung mitochondria of rats exposed to PQ. Male rats were randomly allocated in five groups: Control group, PQ group (50 mg/kg; orally, only on the first day), and PQ + ASA (100, 200, and 400 mg/kg; i.p.) groups for 3 weeks. Mitochondrial indices and respiratory chain-complex activities were determined. PQ induced lung interstitial fibrosis; however, ASA (400 mg/kg) led to decrease in this abnormal alteration. In comparison with PQ group, complex II and IV activity, and adenosine triphosphate content in ASA groups had significantly increased; however, reactive oxygen species production, mitochondrial membrane permeabilization, and mitochondrial swelling were significantly reduced. In conclusion, aspirin can alleviate lung injury induced by PQ poisoning by improving mitochondrial dynamics.

摘要

百草枯(PQ)已在发展中国家导致了众多自杀企图。在百草枯中毒中,阿司匹林(ASA)作为辅助治疗具有改善作用。并且,它在线粒体氧化磷酸化解偶联作用已经得到充分证实。本研究旨在研究暴露于 PQ 的大鼠肺线粒体中阿司匹林的作用机制。雄性大鼠被随机分配到五组:对照组、PQ 组(50mg/kg;仅在第一天口服)和 PQ+ASA(100、200 和 400mg/kg;腹腔注射)组,共 3 周。测定线粒体指数和呼吸链复合物活性。PQ 诱导肺间质纤维化;然而,ASA(400mg/kg)导致这种异常改变减少。与 PQ 组相比,ASA 组的复合物 II 和 IV 活性以及三磷酸腺苷含量显著增加;然而,活性氧的产生、线粒体膜通透性和线粒体肿胀显著减少。总之,阿司匹林可以通过改善线粒体动力学来减轻 PQ 中毒引起的肺损伤。

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