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Suppressive Effect of Chemically Induced Hypoxia on Glioblastoma Cell Proliferation

机译:化学诱导缺氧对胶质母细胞瘤细胞增殖的抑制作用

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摘要

Glioblastoma is a tumor characterized by pronounced hypoxia. Hypoxia produces diverse effects on tumor cells, and the results of experimental studies available so far are contradictory. In vitro hypoxia can be modeled in two ways: by reducing the level of atmospheric oxygen (physically induced hypoxia) or by using hypoxia-inducing chemicals such as cobalt chloride (II) (CoCl2) (chemically induced hypoxia). In the present work, we analyzed the effect of CoCl2 on the viability, proliferation, and apoptosis of cells of three glioblastoma cell lines: 1321N1, T98g, and U373 MG. It was shown that CoCl2 induced a dose-dependent decrease in cell viability and proliferation, and at high concentrations (200 and 400 μM) stimulated cell death. CoCl2 had no effect on the cytotoxic activity of doxorubicin in two cell lines T98g and U373 MG, and enhanced the effect of the chemotherapeutic agent on the 1321N1 cell line, though no synergistic cytotoxic effect of the two agents was observed.
机译:胶质母细胞瘤是一种以明显缺氧为特征的肿瘤。缺氧对肿瘤细胞产生多种影响,迄今为止可用的实验研究结果是矛盾的。体外缺氧可以通过两种方式进行建模:通过降低大气中的氧气水平(物理诱导缺氧)或使用氯化钴 (II) (CoCl2) 等诱导缺氧的化学物质(化学诱导缺氧)。在本研究中,我们分析了CoCl2对3种胶质母细胞瘤细胞系(1321N1、T98g和U373 MG)细胞活力、增殖和凋亡的影响。结果表明,CoCl2诱导细胞活力和增殖的剂量依赖性降低,并且在高浓度(200和400μM)下刺激细胞死亡。CoCl2对两种细胞系T98g和U373 MG中阿霉素的细胞毒性活性没有影响,并增强了化疗药物对1321N1细胞系的作用,但未观察到两种药物的协同细胞毒性作用。

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