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百里醌对砷诱导的大鼠肾脏细胞凋亡和氧化应激的保护作用

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney.

作者信息

Sener Umit, Uygur Ramazan, Aktas Cevat, Uygur Emine, Erboga Mustafa, Balkas Gulseren, Caglar Veli, Kumral Bahadir, Gurel Ahmet, Erdogan Hasan

机构信息

a Department of Physiology , Faculty of Medicine, Namik Kemal University , Tekirdag , Turkey .

b Department of Anatomy , Faculty of Medicine, Namik Kemal University , Tekirdag , Turkey .

出版信息

Ren Fail. 2016;38(1):117-23. doi: 10.3109/0886022X.2015.1103601. Epub 2015 Oct 29.

DOI:10.3109/0886022X.2015.1103601
PMID:26513487
Abstract

We aimed to investigate the protective role of thymoquinone (TQ) by targeting its antiapoptotic and antioxidant properties against kidney damage induced by arsenic in rats. We have used the 24 male Sprague-Dawley rats. Rats were divided into three groups. Physiological serum in 10 mL/kg dose as intragastric was given to the control group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) was given to the arsenic group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) and TQ (10 mg/kg, intragastric by gavage for 15 days) was given to the arsenic + TQ group. After 15 days, the animals' kidneys were taken theirs, then we have performed histological and apoptotic assessment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels have examined as the oxidative stress parameters. We have determined the levels of arsenic. Increased renal injury and apoptotic cells have been detected in the arsenic group. Degenerative changes in the arsenic + TQ group were diminished. Although the MDA levels were augmented in the arsenic group, SOD, CAT and GSH-Px enzyme activities were lessened than the other groups. Our findings suggest that TQ may impede the oxidative stress, the cells have been damaged and also the generation of apoptotic cells arisen from arsenic. TQ plays a protective role against arsenic-induced toxicity in kidney and may potentially be used as a remedial agent.

摘要

我们旨在通过靶向其抗凋亡和抗氧化特性来研究百里醌(TQ)对大鼠砷诱导的肾损伤的保护作用。我们使用了24只雄性Sprague-Dawley大鼠。大鼠被分为三组。对照组给予10 mL/kg剂量的生理血清灌胃。砷组给予亚砷酸钠(10 mg/kg,灌胃15天)。砷+TQ组给予亚砷酸钠(10 mg/kg,灌胃15天)和TQ(10 mg/kg,灌胃15天)。15天后,取出动物的肾脏,然后进行组织学和凋亡评估。检测超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)的酶活性以及丙二醛(MDA)水平作为氧化应激参数。我们测定了砷的含量。砷组检测到肾损伤和凋亡细胞增加。砷+TQ组的退行性变化减少。虽然砷组的MDA水平升高,但SOD、CAT和GSH-Px的酶活性低于其他组。我们的研究结果表明,TQ可能会抑制氧化应激、细胞损伤以及砷引起的凋亡细胞的产生。TQ对砷诱导的肾毒性具有保护作用,可能有潜力用作一种治疗剂。

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