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莪术醇诱导H1650肺癌细胞凋亡的机制探讨 被引量:6

Apoptosis mechanism of H1650 lung cancer cells induced by curcumol
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摘要 目的探究莪术醇对人肺癌H1650细胞增殖抑制与凋亡诱导的作用。方法采用噻唑蓝(MTT)法、Hoechst33258染色、流式细胞术和Western Blot检测莪术醇诱导H1650细胞凋亡的作用及其分子机制。结果 MTT结果显示莪术醇对H1650细胞有明显的增殖抑制作用;Hoechst33258染色后可观察到莪术醇处理后细胞出现"凋亡小体"的特征;流式细胞术检测结果证实了莪术醇能明显的引起H1650细胞凋亡并增加细胞内活性氧的产生;这可能与莪术醇下调JAK2-STAT3信号通路蛋白表达有关。结论莪术醇具有抑制H1650细胞增殖和诱导其凋亡的作用。 Objective To investigate the anti-proliferation and inducing apoptosis effects of curcumol on human lung cancer cell line NCI-H1650. Methods Investigated the curcumol-induced apoptosis activities and mechanism of NCI-H1650 cells through M TT assay,Hoechst 33258 staining,flowcytometry and Western Blot. Results M TT results showed that curcumol had a significant inhibitory effect on NCI-H1650 cells. The apoptotic bodies were observed after curcumol-treatment. The results of flowcytometry showed that curcumol could obviously cause promoting NCI-H1650 cells apoptosis and increase intracellular reactive oxygen species. It was related to curcumol down-regulating JAK2-STAT3 signaling pathway protein expression. Conclusion curcumol inhibits the proliferation and induces apoptosis of H1650 cells.
作者 黎莉莉 郭芳 莫斯喻 臧林泉 LI Lili;GUO Fang;MO Siyu;ZANG Linquan(School of Pharmacology,Guangdong Pharmaceutical University,Guangzhou 510006,China)
出处 《沈阳药科大学学报》 CAS CSCD 北大核心 2019年第2期175-179,共5页 Journal of Shenyang Pharmaceutical University
基金 广东省科技计划资助项目(No 2015A020211028)
关键词 莪术醇 H1650 增殖 凋亡 机制 curcumol H1650 proliferation apoptosis mechanism
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