大蒜素增强脑胶质瘤细胞株U87对TRAIL敏感性的机制研究

Allicin enhances antitumor activity of gliomas cells line U87 to TRAIL

  • 摘要: 目的 研究大蒜素是否能通过增加脑胶质瘤细胞U87对肿瘤坏死因子相关凋亡诱导配体(tumor necrosis factor-related apoptosis-inducing ligand,TRAIL)的敏感性来促进U87细胞的凋亡及其相关机制的研究。 方法 采用MTT法检测大蒜素联合TRAIL对U87细胞活性的影响;流式细胞术(Annexin V/FITC)评估大蒜素联合TRAIL对U87细胞凋亡的影响;Transwell实验进一步检测大蒜素联合TRAIL对U87细胞的侵袭能力的影响;Western-blot、RT-PCR和Q-RT-PCR方法检测大蒜素联合TRAIL对与U87细胞凋亡相关的基因和蛋白的表达影响。 结果 与其他组比较,大蒜素联合TRAIL明显降低U87细胞活力和侵袭能力,促进U87细胞凋亡。在分子水平上,与单独作用组比较,联合作用组明显增加DR4、DR5、Caspase-3和Caspase-8的活性,而AKT、pFKHR、MMP-2和MMP-9的活性明显被抑制。 结论 大蒜素能增强脑胶质瘤细胞U87对TRAIL的敏感性,从而促进U87凋亡。

     

    Abstract: Objective To explore whether allicin can increase the sensitivity of glioma cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis and its mechanism. Methods The effect of allicin combined with TRAIL on cell viability and cell apoptosis of U87 was detected by MTT assay and Annexin V/FITC assay, respectively. The invasive potential of allicin combined with TRAIL to U87 cells was further detected by Transwell experiment, and Western-blot, RT-PCR and Q-RTPCR were used to detect the expression of genes and proteins in allicin combined with TRAIL. Results The synergistic treatment significantly reduced cells viability and invasive activity, while promoted apoptosis in the tested U87 cells. At the molecule level, the synergistic treatment significantly increased the activation of DR4, DR5, caspase-3 and caspase-8, while the expression of AKT, pFKHR, MMP-2 and MMP-9 was significantly inhibited. Conclusion It suggests that allicin can increase the sensitivity of U87 to TRAIL, thus enhancing the apoptosis of U87.

     

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