当前位置: X-MOL 学术J. Biochem. Mol. Toxicol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Concanavalin A induces apoptosis in a dose‐dependent manner by modulating thiol/disulfide homeostasis in C6 glioblastoma cells
Journal of Biochemical and Molecular Toxicology ( IF 3.6 ) Pub Date : 2021-02-18 , DOI: 10.1002/jbt.22742
Fatih Kar 1, 2 , Sedat Kacar 3 , Ceyhan Hacioglu 4 , Gungor Kanbak 2 , Varol Sahinturk 3
Affiliation  

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 500 µg/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 cytokines 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.

中文翻译:

伴刀豆球蛋白A通过调节C6胶质母细胞瘤细胞中的硫醇/二硫键稳态而以剂量依赖性方式诱导凋亡

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。伴刀豆球蛋白A(Con A)具有很多抗肿瘤作用,尤其是在氧化应激时。在本研究中,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,巯基/二硫键稳态,细胞凋亡和炎症的影响。我们通过利用3-(4,5-二甲基噻唑-2-基)-2-,5-二苯基溴化四唑(MTT)检测了C6细胞中Con A的细胞毒性活性(从7.8至500 µg / ml),并确定了毒性找到最佳剂量后,硫醇-二硫化物的体内稳态,总抗氧化剂和氧化剂状态(TAS和TOS),丙二醛(MDA)和谷胱甘肽(GSH)的水平,c(CYCS)和caspase 3(CASP3)被测量。用倒置显微镜和流式细胞仪检测C6细胞的凋亡和形态学变化。剂量依赖性的Con A触发了C6细胞的氧化损伤,影响了炎症途径,因此减少了凋亡蛋白和形态学改变的增殖。但尤其是,Con A通过破坏C6细胞中的硫醇/二硫键平衡来增加二硫键的形成。这项研究表明,Con A被称为碳水化合物结合蛋白,它通过调节C6胶质母细胞瘤细胞中的硫醇/二硫键稳态而以剂量依赖的方式产生氧化损伤,炎症和细胞凋亡。
更新日期:2021-02-18
down
wechat
bug