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Enhancement of taxol-induced apoptosis by inhibition of NF-kB with ursorlic acid

机译:用尿红酸抑制NF-KB抑制紫杉醇诱导的细胞凋亡

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Taxol is known to inhibit cell growth and triggers significant apoptosis in various cancer cells, and activation of proliferation factor NF-B during Taxol-induced apoptosis is regarded as a main reason resulting in tumor cells resistance to Taxol. It has been found that ursorlic acid can inhibit the activation of NF-B. In order to study whether ursorlic acid can enhance the Taxol-induced apoptosis, we use fluorescence resonance energy transfer (FRET) technique and probe SCAT3 to compare the difference of caspase-3 activation between Taxol alone and Taxol combined ursorlic acid. With laser scanning confocal microscopy, we find that ursorlic acid, a nontoxic food component, sensitizes ASTC-a-1 cells more efficiently to Taxol-induced apoptosis by advanced activation of caspase 3. The result also suggests that there would be a synergistic effect between Taxol and ursorlic acid, and the more detailed mechanism of synergistic effect needs to be clarified further, such as the correlations among NF-B, Akt, caspase 8, which leads to the advanced activation of caspase 3 during combined treatment of Taxol and ursorlic acid. Moreover, this may be a new way to improve Taxol-dependent tumor therapy.
机译:已知紫杉醇抑制细胞生长,并触发各种癌细胞中的显着细胞凋亡,并且紫杉醇诱导的细胞凋亡期间的增殖因子NF-B的激活被认为是导致毒素对紫杉醇抗性的主要原因。已经发现尿红酸可以抑制NF-B的活化。为了研究尿红酸是否可以增强紫杉醇诱导的细胞凋亡,我们使用荧光共振能量转移(FRET)技术和探针SCAT3来比较紫杉醇单独和紫杉醇组合尿红酸之间的Caspase-3活化的差异。随着激光扫描共聚焦显微镜,我们发现尿道酸,一种无毒食物组分,通过Caspase 3的先进激活更有效地对紫杉醇诱导的细胞凋亡更有效地敏感ASTC-A-1细胞。结果表明还表明存在协同效应紫杉醇和尿道酸,并且需要进一步澄清更详细的协同效应机制,例如NF-B,AKT,Caspase 8之间的相关性,其导致紫杉醇和鸟素酸组合治疗期间Caspase 3的先进激活。此外,这可能是改善税醇依赖肿瘤疗法的一种新方法。

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