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首页> 外文期刊>Journal of biochemical and molecular toxicology >Concanavalin A induces apoptosis in a dose-dependent manner by modulating thiol/disulfide homeostasis in C6 glioblastoma cells
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Concanavalin A induces apoptosis in a dose-dependent manner by modulating thiol/disulfide homeostasis in C6 glioblastoma cells

机译：通过调节C6胶质母细胞瘤细胞中的硫醇/二硫化物稳态，诱发剂量依赖性方式诱导细胞凋亡

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摘要

Glioma is the most common brain tumor. C6 rat glioblastoma cells provide the possibility to the scientist to study brain cancer. Concanavalin A (Con A) has a lot of antitumoral effects, especially over oxidative stress. In the present study, it was aimed to decide the impacts of various doses of Con A on C6 glioblastoma cells regarding cytotoxicity, thiol/disulfide homeostasis, apoptosis, and inflammation. We detected the cytotoxic activity of Con A (from 7.8 to 500μg/ml) in C6 cells by utilizing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and determined the toxic concentration of Con A. Once the optimal doses were found, the thiol-disulfide homeostasis, levels of total antioxidant and oxidant status (TAS and TOS), malondialdehyde (MDA) and glutathione (GSH), pro-inflammatory cyto-kines as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), apoptotic proteins as cytochrome c (CYCS), and caspase 3 (CASP3) were measured. Apoptotic and morphological changes in the C6 cells were examined with an inverted microscope and flow cytometry technique. Dose-dependent Con A triggered oxidative damage in the C6 cells, affecting the inflammatory pathway, so reducing proliferation with apoptotic proteins and morphological changes. But especially, Con A increased disulfide formation by disrupting the thiol/disulfide balance in C6 cells. This study revealed that Con A, known as carbohydrate-binding protein, generated oxidative damage, inflammation, and apoptosis in a dose-dependent manner by modulating thiol/disulfide homeostasis in C6 glioblastoma cells.
机译：胶质瘤是最常见的脑肿瘤。C6大鼠胶质母细胞瘤细胞为科学家研究脑癌提供了可能性。刀豆球蛋白A（Con A）具有许多抗肿瘤作用，尤其是在氧化应激下。本研究旨在确定不同剂量的Con A对C6胶质母细胞瘤细胞的细胞毒性、硫醇/二硫化物稳态、凋亡和炎症的影响。我们利用3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑溴化铵（MTT）在C6细胞中检测Con A（7.8至500μg/ml）的细胞毒性活性，并测定Con A的毒性浓度。一旦找到最佳剂量，硫醇二硫化物稳态、总抗氧化和氧化状态（TAS和TOS）、丙二醛（MDA）和谷胱甘肽（GSH）水平，检测促炎细胞因子如肿瘤坏死因子α（TNF-α）和白细胞介素6（IL-6）、凋亡蛋白如细胞色素c（CYCS）和半胱天冬酶3（CASP3）。用倒置显微镜和流式细胞术检测C6细胞的凋亡和形态学变化。剂量依赖性Con A在C6细胞中引发氧化损伤，影响炎症途径，从而通过凋亡蛋白和形态学改变减少增殖。但尤其是，Con通过破坏C6细胞中硫醇/二硫键的平衡而增加了二硫键的形成。这项研究表明，被称为碳水化合物结合蛋白的Con A通过调节C6胶质母细胞瘤细胞中硫醇/二硫化物的稳态，以剂量依赖性的方式产生氧化损伤、炎症和凋亡。

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