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作 者:邱建[1] 傅云峰[1] 程琪[1] 程晓东[1] 谢幸[1] 吕卫国[1]
机构地区:[1]浙江大学医学院附属妇产科医院肿瘤科,浙江省女性生殖健康研究重点实验室,杭州310006
出 处:《中华医学杂志》2012年第27期1926-1928,共3页National Medical Journal of China
基 金:国家自然科学基金(30901591);浙江省151卫生高层次创新人才培养工程项目
摘 要:目的研究姜黄素对卵巢癌耐紫杉醇细胞SKOV3-TR30的耐药性的逆转作用及可能机制。方法应用噻唑蓝比色法及流式细胞检测姜黄素和(或)紫杉醇作用后SKOV3-TR30细胞增殖及细胞周期的改变;Western印迹法检测GSK-3蛋白表达变化。结果姜黄素显著降低了紫杉醇对SKOV3-TR30细胞的IC50逆转倍数达3.0倍;细胞周期分析显示,只有(27.0±2.9)%的SKOV3-TR30细胞被紫杉醇阻滞在G2-M期,而(78.5±6.4)%的SKOV3-TR30细胞被姜黄素联合紫杉醇阻滞在G2-M期;姜黄素作用12、24h后SKOV3-TR30中GSK-3蛋白表达水平显著下调。结论低细胞毒剂量姜黄素可部分逆转SKOV3-TR30细胞对紫杉醇的耐药性,下调GSK-3蛋白表达可能是其发挥逆转作用的机制之一。Objective To explore the effects of curcumin on paclitaxel resistance reversal of SKOV3-TR30 cell line and its mechanism. Methods The (3-(4, 5-dimethyhhiazol-2-yl)-2, 5- diphenyhetrazolium bromide) MTT assay was performed to determine the sensitivity of curcumin-treated SKOV3-TR30 cells to paclitaxel. The cell cycle distribution of SKOV3-TR30 was analyzed by flow cytometry. And the expression level of glycogen synthase kinase-3 (GSK-3) protein was detected by Western blot. Results IC50 of paclitaxel in SKOV3-TR30 decreased with a treatment of curcumin. And the reversal times was 3.0. Flow cytometric analysis of curcumin-treated SKOV3-TR30 cells demonstrated a distinct G2-M phase block (78. 5 ± 6.4) % after a 12-hour treatment of paclitaxel versus SKOV3-TR30 cells without curcumin. There was a lack of G2-M phase arrest ( only 27.0%± 2.9% ). The expression of GSK-3 protein in SKOV3-TR30 cells decreased with the 12 and 24-hour treatments of curcumin. Conclusion Curcumin can partially reverse the paclitaxel-resistance of SKOV3-TR30 cells through a down-regulation of GSK-3.
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