| 李云波,金哲.清毒栓含药血清对宫颈癌SiHa细胞MDM2基因的影响[J].,2007,(2):147-150 |
| 清毒栓含药血清对宫颈癌SiHa细胞MDM2基因的影响 |
| Effect of Qingdu Suppository-containing Serum on Cervical Carcinoma SiHa Cell MDM2 Gene Expression |
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| DOI： |
| 中文关键词: 清毒栓含药血清 宫颈癌SiHa细胞 MDM2 |
| 英文关键词:Qingdu Suppository-containing serum cervical carcinoma SiHa cell MDM2 |
| 基金项目:2005年博士学科点科研基金课题(中药对宫颈癌细胞PTEN-MDM2-P53网络及泛素化影响No.20050026003) |
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| 中文摘要: |
| 目的研究中药清毒栓对宫颈癌SiHa细胞生长的调节作用,从细胞生物学及分子生物学水平探讨清毒栓对抑制宫颈癌SiHa细胞生长的作用机制。方法以不同浓度清毒栓含药血清培养液作用于SiHa细胞,并设立空白血清及含中、西药阳性对照药血清为对照,通过MTT法检测清毒栓对细胞生长增殖的影响;用流式细胞分析技术进行细胞周期及细胞凋亡检测,并用RT-PCR法半定量检测原癌基因MDM2表达。结果经清毒栓含药8%的血清培养液作用后细胞数量减少,其中以血清作用72h时对细胞抑制作用最强,与空白组比较,差异有显著性(P<0.01);细胞周期各时相中,清毒栓含药血清S期细胞所占的比例明显减少,对细胞凋亡有影响,但未见明显规律性,RT-PCR结果示清毒栓含药血清细胞中MDM2表达明显减少。结论清毒栓含药血清不仅可直接抑制宫颈癌细胞的生长,并可能通过下调MDM2基因表达的分子机制,达到抑制肿瘤的目的。 |
| 英文摘要: |
| ObjectiveTo investigate the effect and mechanism of Qingdu Suppository(QDS)in suppressing the growth of SiHa cell of cervical carcinoma on the cytobiologic and molecular biologic level.Methods SiHa cells were cultured in media with serum containing different concentrations of QDS and blank serum,as well as serum containing various Chinese herbal or Western drugs as positive control.SiHa cell growth and proliferation was determined by MTT assay,the cell cycle and apoptosis were analyzed by flow cytometry technique,and the expression of proto-oncogene MDM2 detected semi-quantitatively by RT-PCR.ResultsThe amount of cells decreased after cultured with drug-containing serum 8% in concentration,with the highest inhibitory effect shown by drug-containing serum after acting for 72 h,which was significantly different to that in the control group(P<0.01).Among the various time phases of cell cycle,the percentage of cells in S phase was significantly decreased.Drug-containing serum showed somewhat effect on cell apoptosis,but no obvious regularity could be found.RT-PCR showed significant decrease of MDM2 expression.ConclusionQDS containing serum could not only directly suppress the growth of cervical carcinoma cells,but also inhibit the tumor by the molecular mechanism of down-regulating MDM2 gene expression. |
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