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作 者:马静[1] 赵雯红[1] 袁世发[2] 黄丽珍[1] 张佳佳[3] 程建新[1]
机构地区:[1]河北医科大学第四医院妇科,石家庄050011 [2]河北武警总队医院普外科,石家庄050038 [3]北京大学第三医院妇产科,北京100191
出 处:《现代妇产科进展》2016年第7期515-517,522,共4页Progress in Obstetrics and Gynecology
基 金:河北省卫生和计划生育委员会医学科学研究重点课题(No:20150337)
摘 要:目的:探讨NK-1受体拮抗剂对子宫内膜癌Ishikawa细胞增殖、凋亡、细胞周期及侵袭影响。方法:体外培养子宫内膜腺癌Ishikawa细胞,将不同浓度NK-1受体拮抗剂与其共培养48h后,采用MTT法检测Ishikawa细胞增殖情况;采用流式细胞术检测细胞凋亡率及细胞周期分布;利用Transwell实验检测细胞侵袭能力。结果:NK-1受体拮抗剂可明显抑制Ishikawa细胞增殖(P<0.05);促进细胞凋亡,使细胞周期中G0/G1期比例增加,S期及G2/M期比例降低(P均<0.05);抑制细胞侵袭,并且其对Ishikawa细胞的这些作用均呈剂量依赖性。结论:NK-1受体拮抗剂可明显抑制子宫内膜癌细胞增殖、阻滞细胞周期、诱导凋亡及抑制侵袭,有望成为子宫内膜细胞治疗的新途径。Objective: To investigate the effects of NK-1 receptor antagonist( L-33,060) on proliferation,apoptosis,cell cycle and invasion of human endometrial adenocarcinoma Ishikawa cells. Methods: Human endometrial adenocarcinoma Ishikawa cells were cultured in vitro and treated with different concerration of L-33,060 for 48 h respectively. MTT assay and flow cytometry were used to measure the effects of L-33,060 on cell proliferation and cell cycle.The activity of invasion was analyzed by Transwell assay. Results: L-33,060 inhibited cell proliferation of cultured Ishikawa cells( P < 0. 05). L-33,060 blocked the cycle in G0 ~ G1 period and increased the rates of cell apoptosis( P<0. 05). The activity of invasion was inhitited by L-33,060( P<0. 05). All the effects were in a dose dependent manner. Conclusion: The NK-1 receptor antagonist could inhibit cell proliferation,block cell cycles,induce cell apoptosis and arrest invasion. It would become a new therapies for endmetrial carcinoma.
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