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作 者:徐秀莲[1] 陈声利[1] 陈浩[1] 姜祎群[1] 曾学思[1] 孙建方[1]
机构地区:[1]中国医学科学院,中国协和医科大学皮肤病研究所,江苏南京210042
出 处:《临床皮肤科杂志》2007年第4期204-207,共4页Journal of Clinical Dermatology
基 金:国家教委高校博士点基金资助项目(20030023055)
摘 要:目的:研究紫杉醇对皮肤T细胞淋巴瘤(cutaneous T cell lymphoma,CTCL)Hut78细胞株的生长抑制及诱导凋亡作用,并探讨其诱导凋亡作用的机制。方法:将紫杉醇按不同浓度、不同作用时间分别处理Hut78细胞,四甲基偶氮唑蓝(MTT)法测定Hut78细胞的生长抑制率,端粒酶重复序列扩增及酶联免疫吸附法(TRAP-PCR-ELISA)检测端粒酶活性的变化,采用形态学观察和流式细胞仪检测其诱导Hut78细胞凋亡的情况。结果:紫杉醇明显下调端粒酶活性表达,对Hut78细胞具有生长抑制及诱导凋亡的作用,且呈时间依赖和剂量依赖性。表现为G2/M期阻滞,出现典型的凋亡细胞特征,流式细胞仪检测可见明显的凋亡峰。结论:紫杉醇能下调端粒酶的活性,诱导细胞凋亡是其发挥抗癌作用的机制之一。Objective: To observe the effects of paclitaxel on apoptosis induction in cutaneous T-cell lymphoma cell line Hut78 in vitro. Methods: Hut78 was treated by paclitaxel with different concentration and acting time. Telomerase activity was determined by TRAP-PCR-ELISA. The inhibition of Hut78 cell growth was measured by MTr assay. The apoptosis of Hut78 was examined by flow cytometry. Results: Paclitaxel could down-regulate telomerase activity, inhibit the growth of Hut78, and induce cell apoptosis in a dose and time dependent manner. S phase and G2/M phase DNA content increased and a typical subdiploid peak before G0/G1 phase were observed by flow cytometry. Conclusions: Paclitaxel has obvious effects of growth-inhibiting on cutaneous T-cell lymphoma and can induce apoptosis of Hut78 cell.
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