期刊文献+

菟丝子醇提物对胃癌SGC7901细胞的生长抑制作用研究 被引量:7

Inhibition of Cuscuta Chinenssis Lam on Human Gastric Cancer SGC7901 Cell
下载PDF
导出
摘要 目的探讨菟丝子(CCL)醇提物对人胃癌SGC7901细胞生长的抑制作用。方法以不同浓度(10、50、100 mg/L)的菟丝子作用于人胃癌SGC7901细胞,同时设二甲基亚砜(DMSO)和RPMI1640培养液作为对照组。采用噻唑蓝(MTT)法检测菟丝子对人胃癌SGC7901细胞的生长抑制情况,通过对SGC7901细胞周期测定,探讨菟丝子对细胞增殖作用的影响。结果菟丝子对SGC7901细胞生长有明显抑制作用,且随着剂量的增高(10~100 mg/L)及作用时间的延长,细胞增殖抑制率亦增高(P〈0.01)。100 mg/L的菟丝子作用不同时间(12、24、36 h),处于G0/G1期、S期的细胞所占百分率比较,差异有统计学意义(P〈0.01)。结论菟丝子醇提取物能够抑制人胃癌SGC7901细胞的生长。可能是通过影响人胃癌SGC7901细胞内DNA复制和合成,抑制细胞正常分裂,阻滞细胞进入S期,从而使细胞在G1期堆积,出现G2/M期阻滞,有丝分裂终止,从而抑制细胞增殖。 Objective To study the effect of Cuscuta chinenssis Lam(CCL) on inhibiting human gastric cancer SGC7901 cell.Methods Human gastric cancer SGC7901 cell line was affected by CCL with different concentration(10,50,100 mg/L),meanwhile,the DMSO and RPMI1640 culture liquid was taken as the control group.The inhibition of CCL on SGC7901 cells was detected by MTT method.By testing the cell cycle of SGC7901,the effect of CCL on cell proliferation was studied.Results CCL inhibited significantly the growth of SGC7901 cells,and the inhibition increased when the dosage was raised(10~100 mg/L) and the time was extended(P0.01).When SGC7901 cells in stage G0/G1 and stage S were affected by 100 mg/L CCL,the differences were significant when the time changed(12,24,36 h)(P0.01).Conclusion CCL could inhibit human gastric cancer SGC7901 cell.CCL could inhibit tumor cell replication and DNA synthesis,inhibit normal cell division,and stop cell enter S phase,so that cells are accumulated in G1 period with G2/M block to prevented cell mitosis,thereby cell proliferation is inhibited,which lead to tumor cell apoptosis.
出处 《中国全科医学》 CAS CSCD 北大核心 2011年第6期675-676,682,共3页 Chinese General Practice
基金 黑龙江省卫生厅资助项目(2007-501)
关键词 菟丝子 胃肿瘤 SGC7901细胞 细胞凋亡 Cuscuta chinensis Stomach neoplasms SGC7901 cell Apoptosis
  • 相关文献

参考文献4

  • 1Lee KH. Novel antitumor agents from higher plants [J]. Med Res Rev, 1999,19(6):569-596.
  • 2Abal M, Andreu JM, Barasoain I. Taxanes: microtubule and centrosome targets, and cell cycle dependent mechanisms of action [J]. Curr Cancer Drug Targets, 2003, 3:193-203.
  • 3Desagher S, Osensand A, Nichols A, et al. Bid induced conformational change of Bax is responsible for mitochondrial cytoch rome C release during apoptosis [J]. J Cell Biol, 1999, 144 (3): 891-901.
  • 4Sausville EA. Cyclindependent kinase modulators studied at the NCI : preclinical and clinical studies [J]. Curr Med Chem AntiCanc Agents, 2003, 3 (1): 47-56.

同被引文献197

引证文献7

二级引证文献39

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部