文章摘要
吕怡凝,刘天华,彭燕丽,刘真宏,王 璐,单宏丽.蛇床子素促进人骨肉瘤细胞株SAOS-2凋亡[J].,2017,17(11):2012-2015
蛇床子素促进人骨肉瘤细胞株SAOS-2凋亡
Osthole Promotes the Apoptosis of Human Osteosarcoma Cell Line SAOS-2
投稿时间:2016-06-28  修订日期:2016-07-25
DOI:10.13241/j.cnki.pmb.2017.11.003
中文关键词: 蛇床子素  人骨肉瘤细胞  细胞凋亡
英文关键词: Osthole  Human Osteosarcoma Cells  Cell Apoptosis
基金项目:黑龙江省自然科学基金项目(QC2016120)
作者单位E-mail
吕怡凝 哈尔滨医科大学药理教研室 黑龙江 哈尔滨 150081哈尔滨市社会保险事业管理局医院 黑龙江 哈尔滨 150081 lyn29899188@126.com 
刘天华 哈尔滨医科大学药理教研室 黑龙江 哈尔滨 150081  
彭燕丽 哈尔滨医科大学药理教研室 黑龙江 哈尔滨 150081  
刘真宏 哈尔滨医科大学药理教研室 黑龙江 哈尔滨 150081  
王 璐 哈尔滨医科大学药理教研室 黑龙江 哈尔滨 150081  
单宏丽 哈尔滨医科大学药理教研室 黑龙江 哈尔滨 150081  
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中文摘要:
      摘要 目的:观察蛇床子素(osthole)对人骨肉瘤细胞SAOS-2增殖和凋亡的影响及潜在的调控机制。方法:采用MTT法、TUNEL染色技术和流式细胞术检测不同浓度蛇床子素对骨肉瘤细胞凋亡的影响;Western blot检测蛇床子素对骨肉瘤细胞中与细胞凋亡密切相关的蛋白(Bax、Bcl-2)的变化。结果:蛇床子素作用于SAOS-2细胞后,MTT结果显示SAOS-2细胞的活力受到明显抑制,且与蛇床子素浓度和时间相关;Western blot结果显示细胞中的促凋亡蛋白Bax表达上调,抗凋亡蛋白Bcl-2表达明显减弱,且呈剂量依赖性。结论:蛇床子素可显著抑制人骨肉瘤细胞的增殖且促进其凋亡的作用,可能与上调凋亡蛋白Bax和下调抗凋亡蛋白Bcl-2的表达有关。
英文摘要:
      ABSTRACT Objective: To explore the effects induced by osthole on the proliferation and apoptosis of human osteosarcoma cell line SAOS-2 and the involved control mechanism. Methods: After SAOS-2 cells were incubated with different concentrations of osthole, apoptosis of SAOS-2 cells was detected by MTT, TUNEL and flow cytometry assays. The expression of apoptosis associated proteins (Bax and Bcl-2) was determined by Western blot. Results: The results of MTT showed that osthole inhibited the vitality of SAOS-2 cells in a dose-and time-dependent manner. The results of Western blot showed that osthole up-regulated the expression of apoptotic protein Bax remarkably, but decreased the level of anti-apoptotic protein Bcl-2 significantly. Moreover, the regulation on Bax and Bcl-2 protein were associated with the dose of osthole. Conclusion: Osthole inhibits proliferation and promotes cell apoptosis in SAOS-2 cells. The up-regulation of apoptotic protein Bax and down-regulation of anti-apoptotic protein Bcl-2 may be involved in the osthole induced apop- tosis in SAOS-2 cells.
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