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槲皮素对尼古丁诱导的“HepG2细胞”氧化应激的保护作用。

Protective effects of quercetin on nicotine induced oxidative stress in 'HepG2 cells'.

作者信息

Yarahmadi Amir, Zal Fatemeh, Bolouki Ayeh

机构信息

a Biochemistry Department, School of Medicine , Shiraz University of Medical Sciences , Shiraz , Iran.

b Infertility Research Center , Shiraz University of Medical Sciences , Shiraz , Iran.

出版信息

Toxicol Mech Methods. 2017 Oct;27(8):609-614. doi: 10.1080/15376516.2017.1344338. Epub 2017 Jul 18.

DOI:10.1080/15376516.2017.1344338
PMID:28627253
Abstract

Nicotine is a natural component of tobacco plants and is responsible for the addictive properties of tobacco. Nicotine has been recognized to result in oxidative stress by inducing the generation of reactive oxygen species (ROS). The purpose of this work was to estimate the hepatotoxicity effect of nicotine on viability and on antioxidant defense system in cultures of HepG2 cell line and the other hand, ameliorative effect of quercetin (Q) as an antioxidant was analyzed. Nicotine induced concentration dependent loss in HepG2 cell line viability. The results indicated that nicotine decreased activity of superoxide dismutase (SOD) and glutathione reductase (GR) and increased activities of catalase (CAT) and glutathione peroxidase (GPx) and glutathione (GSH) content in the HepG2 cells. Q significantly increased activity of SOD, GR and GSH content and decreased activity of GPX in nicotine + Q groups. Our data demonstrate that Q plays a protective role against the imbalance elicited by nicotine between the production of free radicals and antioxidant defense systems, and suggest that administration of this antioxidant may find clinical application where cellular damage is a consequence of ROS.

摘要

尼古丁是烟草植物的天然成分,是烟草具有成瘾性的原因。人们已经认识到,尼古丁会通过诱导活性氧(ROS)的产生而导致氧化应激。这项工作的目的是评估尼古丁对HepG2细胞系培养物活力和抗氧化防御系统的肝毒性作用,另一方面,分析了抗氧化剂槲皮素(Q)的改善作用。尼古丁诱导HepG2细胞系活力呈浓度依赖性丧失。结果表明,尼古丁降低了超氧化物歧化酶(SOD)和谷胱甘肽还原酶(GR)的活性,增加了过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)的活性以及HepG2细胞中谷胱甘肽(GSH)的含量。在尼古丁+Q组中,Q显著增加了SOD、GR的活性和GSH的含量,并降低了GPX的活性。我们的数据表明,Q对尼古丁引起的自由基产生与抗氧化防御系统之间的失衡起到保护作用,并表明在细胞损伤是由ROS导致的情况下,这种抗氧化剂的给药可能具有临床应用价值。

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