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目的探讨甘草查尔酮A(LCA)对人胶质瘤U87、U251细胞的增殖抑制和促凋亡作用及其机制研究。方法通过四甲基偶氮唑蓝(MTT)比色法检测细胞增殖抑制作用,并计算出半数抑制浓度(IC50),按IC50和100μM不同浓度进行分组。采用倒置显微镜观察细胞形态,流式细胞术检测细胞凋亡以及Western Blot从蛋白水平检测凋亡相关分子的改变情况。结果 MTT显示LCA对人胶质瘤U87、U251细胞具有明显的增殖抑制作用,呈浓度及时间依赖性,LCA对U87、U251细胞48 h的IC50值分别为61.54μM和53.02μM,倒置显微镜下观察细胞密度减少,形态发生明显改变。流式细胞术结果显示,LCA可促进胶质瘤U87、U251的细胞凋亡(P<0.01)。Western Blot结果显示,LCA干预后可显著降低胶质瘤U87、U251细胞内Bcl-2的表达(P<0.01),相反,增加Bax的表达(P<0.05),呈浓度依赖性。结论 LCA对胶质瘤U87、U251细胞具有明显的增殖抑制作用,可能通过内源性凋亡途径诱导其凋亡。
Objective To investigate the effects of licochalcone A (LCA) on the proliferation and apoptosis of human glioma U87 and U251 cells and its mechanism. Methods MTT assay was used to detect the cell proliferation inhibitory effect. IC50 was calculated and divided into groups according to the concentration of IC50 and 100μM. The morphological changes of the cells were observed by inverted microscope, apoptosis was detected by flow cytometry and Western Blot was used to detect the changes of apoptosis-related molecules from the protein level. Results MTT showed that LCA had a significant inhibitory effect on human glioma U87 and U251 cells in a concentration- and time-dependent manner. The IC50 values of LCA for U87 and U251 cells for 48 h were 61.54 μM and 53.02 μM, respectively. Under inverted microscope Decreased cell density, morphological changes significantly. Flow cytometry showed that LCA could promote the apoptosis of glioma U87 and U251 cells (P <0.01). Western Blot showed that LCA could significantly decrease the expression of Bcl-2 in glioma U87 and U251 cells (P <0.01), and increase the expression of Bax (P <0.05) in a concentration-dependent manner. Conclusion LCA has obvious proliferation inhibition on glioma U87 and U251 cells, which may induce apoptosis through endogenous apoptosis pathway.