摘要
目的:探讨百里醌对人卵巢癌细胞株OVCAR-3的作用及相关机制。方法:采用不同浓度(0、10μmol/L、20μmol/L和40μmol/L)百里醌处理OVCAR-3细胞。MTT法检测细胞增殖活性,流式细胞仪检测细胞凋亡。RT-PCR和ELISA检测炎症因子白介素-6(IL-6)、白介素1β(IL-1β)和肿瘤坏死因子-α(TNF-α)表达水平。Western blot法检测JAK2、STAT3、p-JAK2、p-STAT3、p-p65和p65表达。结果:百里醌呈浓度依赖性抑制OVCAR-3细胞的增殖和诱导OVCAR-3凋亡,降低IL-6、IL-1β、TNF-α、p-JAK2、p-STAT3和p-p65表达,而对JAK2、STAT3和p65表达无影响。结论:百里醌可抑制OVCAR-3细胞的增殖和诱导凋亡,其作用机制与抑制JAK2/STAT3/p65介导的炎症相关。
Objective:To investigate the effect and mechanisms of the thymoquinone on human ovarian cancer cell line OVCAR-3.Methods:The OVCAR-3 cell were treated with different concentration of thymoquinone.The proliferation activity of OVCAR-3 was detected by MTT assay,and the apoptosis of OVCAR-3 was exanimed by Flow cytometry.The expression Levels of TNF-α,IL-6 and IL-1β were meaured by ELISA and RT-PCR.The protein level of JAK2、STAT3、p-JAK2,p-STAT3,p-p65 and p65 were exanimed by Western blotting.Results:The results showed that thymoquinone can induce the proliferation inhibition and apoptosis of OVCAR-3 with the downregluating the expressions of IL-6,IL-1β,TNF-α,p-JAK2,pSTAT3 and p-p65 in OVCAR-3 cell in a dose-dependent manner and no inflence on the expression of JAK2、STAT3 and p65.Conclusion:Thymoquinone can induce apoptosis and growth inhibition of OVCAR-3 cell which is associated with suppressing JAK2/STAT3/p65 mediating inflammation.
出处
《现代妇产科进展》
CSCD
北大核心
2016年第5期345-348,共4页
Progress in Obstetrics and Gynecology
基金
宜昌市基金(No:A11301-38)
