二甲双胍对胶质母细胞瘤细胞的抑制作用研究

为了探究二甲双胍对不同胶质母细胞瘤U87细胞、GL261细胞及C6细胞增殖的影响，选取小鼠GBM细胞GL261细胞系、大鼠GBM细胞C6细胞系及人源GBM细胞U87MG细胞系，使用二甲双胍处理，通过CCK-8法检测细胞增殖活性；细胞实时荧光检测细胞凋亡水平；平板克隆实验检测GBM细胞克隆形成能力；CCK-L法检测胞内ATP水平；Western blot检测Akt及其磷酸化水平。结果显示，与对照组相比，随着作用浓度增加，二甲双胍显著抑制GBM细胞增殖活性，影响细胞形态；与对照组相比，同一作用浓度下，二甲双胍提高了GBM细胞凋亡水平，抑制了GBM细胞克隆形成能力，降低了GBM胞内ATP的产生；二甲双胍处理24 h后，GBM细胞内p-Akt表达显著下调，Akt无明显变化。结果表明，二甲双胍在体外可抑制多种GBM细胞的增殖、克隆，降低胞内ATP水平，其机制可能与Akt磷酸化水平相关，研究结果为进一步探索二甲双胍对胶质母细胞瘤的作用机制提供了体外研究理论基础。

Inhibitory Effect of Metformin Hydrochloride on Glioblastoma Cells

The aim of this study was to explore the effect of metformin hydrochloride on the proliferation of different glioblastoma U87 cells， GL261 cells and C6 cells， a mouse GBM cell line GL261， a rat GBM cell line C6 and a human GBM cell line U87MG were selected and treated with metformin hydrochloride. The cell proliferative activity was detected by CCK-8 method； cell apoptosis level was detected by cell real-time fluorescence detection； the clonal formation ability of GBM cells was detected by plate cloning experiment； the intracellular ATP level was detected by CCK-L method； Akt and its phosphorylation were detected by Western blot. Results showed that， compared with the control group， metformin hydrochloride significantly inhibited the proliferative activity of GBM cells and affected cell morphology with the increase of the concentration. Compared with the control group， at the same concentration， metformin hydrochloride increased the apoptotic level of GBM cells， inhibited the clonal formation ability of GBM cells， and reduced the production of ATP in GBM cells. After 24 h of metformin hydrochloride treatment， the p-Akt expression in GBM cells was significantly down-regulated， but there was no significant change in Akt. The results showed that metformin hydrochloride could inhibit the proliferation and clonal formation of a variety of GBM cells and reduce the intracellular ATP level in vitro， which might be related to the phosphorylation of Akt. The results was expected to provide a theoretical basis for further research on the mechanism of metformin hydrochloride against glioblastoma in vitro.