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硒对氟诱导的细胞凋亡和氧化应激发挥保护作用,并改变 Bcl-2/Caspase 家族的表达。

Selenium Exerts Protective Effects Against Fluoride-Induced Apoptosis and Oxidative Stress and Altered the Expression of Bcl-2/Caspase Family.

机构信息

Laboratory Animal Center, Shanxi Key Laboratory of Experimental Animal Science and Human Disease Animal Model, Shanxi Medical University, Road Xinjian 56, Taiyuan, 030001, China.

Shanxi Key Laboratory of Ecological Animal Science and Environmental Medicine, Shanxi Agricultural University, Taigu, 030801, China.

出版信息

Biol Trace Elem Res. 2021 Feb;199(2):682-692. doi: 10.1007/s12011-020-02185-w. Epub 2020 Jul 1.

DOI:10.1007/s12011-020-02185-w
PMID:32613488
Abstract

Fluoride is widely distributed in nature, and at high concentrations, it targets the kidney and especially proximal tubule epithelial cells. Selenium is a typical trace element beneficial to humans, and the role of selenium in the prevention and treatment of fluoride-induced organ damage is an important research topic. The purpose of this study was to investigate the possible protective effects of selenium against fluoride-induced oxidative stress and apoptosis in rat renal tubular epithelial cells. We showed that the activity of antioxidant enzymes (superoxide dismutase and glutathione peroxidase) and total antioxidant capacity were significantly reduced in NaF-treated normal rat kidney cells (NRK-52E), whereas the levels of nitrogen monoxide (NO) and malondialdehyde (MDA) were significantly increased. Moreover, the number of apoptotic cells, mRNA expression of Bax, Bad, caspase-3, caspase-8, and caspase-9, and protein expression of Bax were elevated, while mitochondrial membrane potential and the protein expression of Bcl-2 were reduced. Compared with the NaF group, pretreatment with selenium enhanced the activity of antioxidant enzymes, mitochondrial membrane potential, and protein expression of Bcl-2, while the levels of NO and MDA, number of apoptotic cells, mRNA expression of Bax, Bad, caspase-3, caspase-8, and caspase-9, and protein expression of Bax were decreased. In conclusion, selenium exerted remarkable protective effect against NaF-induced oxidative stress and apoptosis and altered the expression of Bcl-2/caspase family.

摘要

氟广泛存在于自然界中,在高浓度下,它以肾脏为靶器官,特别是近端肾小管上皮细胞。硒是一种对人体有益的典型微量元素,硒在预防和治疗氟化物诱导的器官损伤中的作用是一个重要的研究课题。本研究旨在探讨硒对氟化物诱导的大鼠肾小管上皮细胞氧化应激和细胞凋亡的可能保护作用。结果表明,在 NaF 处理的正常大鼠肾细胞(NRK-52E)中,抗氧化酶(超氧化物歧化酶和谷胱甘肽过氧化物酶)的活性和总抗氧化能力显著降低,而一氧化氮(NO)和丙二醛(MDA)的水平显著升高。此外,凋亡细胞数量、Bax、Bad、caspase-3、caspase-8 和 caspase-9 的 mRNA 表达以及 Bax 蛋白表达升高,而线粒体膜电位和 Bcl-2 蛋白表达降低。与 NaF 组相比,硒预处理增强了抗氧化酶的活性、线粒体膜电位和 Bcl-2 蛋白表达,而 NO 和 MDA 水平、凋亡细胞数量、Bax、Bad、caspase-3、caspase-8 和 caspase-9 的 mRNA 表达以及 Bax 蛋白表达降低。总之,硒对 NaF 诱导的氧化应激和细胞凋亡具有显著的保护作用,并改变了 Bcl-2/caspase 家族的表达。

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