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化学诱导性缺氧对胶质母细胞瘤细胞增殖的抑制作用

Suppressive Effect of Chemically Induced Hypoxia on Glioblastoma Cell Proliferation.

作者信息

Kholodenko I V, Yarygin K N

机构信息

V. N. Orekhovich Research Institute of Biomedical Chemistry, Moscow, Russia.

出版信息

Bull Exp Biol Med. 2023 Aug;175(4):530-534. doi: 10.1007/s10517-023-05900-4. Epub 2023 Sep 28.

Abstract

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) (CoCl) (chemically induced hypoxia). In the present work, we analyzed the effect of CoCl on the viability, proliferation, and apoptosis of cells of three glioblastoma cell lines: 1321N1, T98g, and U373 MG. It was shown that CoCl induced a dose-dependent decrease in cell viability and proliferation, and at high concentrations (200 and 400 μM) stimulated cell death. CoCl 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.

摘要

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,而目前现有的实验研究结果相互矛盾。体外缺氧可以通过两种方式模拟:降低大气氧水平(物理诱导缺氧)或使用缺氧诱导化学物质,如氯化钴(II)(CoCl)(化学诱导缺氧)。在本研究中,我们分析了CoCl对三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,CoCl诱导细胞活力和增殖呈剂量依赖性下降,在高浓度(200和400μM)时刺激细胞死亡。CoCl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,并且增强了化疗药物对1321N1细胞系的作用,尽管未观察到两种药物的协同细胞毒性作用。

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