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目的 探讨NF κB在紫杉醇诱导肿瘤细胞凋亡中的作用及小白菊内酯对紫杉醇诱导凋亡的影响。方法 以人乳癌BCap37细胞和人表皮KB细胞为研究对象 ,用 5,1 0和 2 0 μmol·L-1 小白菊内酯预处理细胞 ,以DNA凋亡梯状条带、DNA含量、MTT、细胞甩片及电泳迁移率变动分析 (EMSA)法检测它对紫杉醇诱导细胞凋亡的影响并探索其作用靶点。结果 通过检测DNA凋亡梯状条带、DNA含量和细胞生存率 ,2 0μmol·L-1 小白菊内酯能显著抑制紫杉醇所诱导的BCap37和KB细胞凋亡 ,但不影响紫杉醇诱导肿瘤细胞G2 /M期阻滞。EMSA实验表明小白菊内酯能抑制紫杉醇诱导激活NF κB。结论 小白菊内酯通过抑制NF κB的激活来抑制紫杉醇所诱导的肿瘤细胞凋亡 ,而紫杉醇诱导肿瘤细胞凋亡的过程可能与G2 /M期阻滞无关
Objective To investigate the role of NF-κB in paclitaxel-induced tumor cell apoptosis and the effects of parthenolide on paclitaxel-induced apoptosis. Methods Human breast cancer BCap37 cells and human epidermal KB cells were treated with 5, 100 and 20 μmol·L-1 parthenolide to pretreat the cells, DNA ladder, DNA content, MTT, The influence of paclitaxel on cell apoptosis induced by Paclitaxel and its target were detected by EMSA. Results DNA fragmentation and cell viability were detected by DNA ladder, DNA content and cell viability. 20 μmol·L-1 parthenolide significantly inhibited paclitaxel-induced apoptosis in BCap37 and KB cells but did not affect paclitaxel-induced tumor cell G2 / M block. EMSA experiments showed that parthenolide could inhibit paclitaxel-induced NFκB activation. Conclusions Parthenolide can inhibit paclitaxel-induced tumor cell apoptosis by inhibiting the activation of NF-κB, whereas paclitaxel-induced tumor cell apoptosis may not be related to G2 / M arrest