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大蒜素协同抗癌药对肿瘤细胞杀伤作用的研究
引用本文:哈敏文, 董明, 王兰, 袁媛. 大蒜素协同抗癌药对肿瘤细胞杀伤作用的研究[J]. 中国肿瘤临床, 2004, 31(4): 193-196.
作者姓名:哈敏文  董明  王兰  袁媛
作者单位:中国医科大学附属第一医院肿瘤研究所第三研究室 沈阳市110001
基金项目:国家重点基础研究发展计划(973计划)
摘    要:目的:探讨大蒜素对人胃癌细胞系MGC-803和SGC-7901细胞周期的影响及其与周期特异性药物联合使用,增强抗癌药物对肿瘤细胞的杀伤作用。方法:苔盼蓝拒染法检测细胞增殖抑制率以观察大蒜素对胃癌细胞的增殖抑制作用;流式细胞仪及瑞士-姬姆萨染色光镜观察检测细胞周期的改变;3μg/ml大蒜素与周期特异性抗癌药物博莱霉素A5和长春新碱联合使用,观察药物细胞毒活性的改变。结果:大蒜素可抑制MGC-803细胞生长,24hIC50为6.4μg/ml,也可抑制SGC-7901细胞的生长,24hIC50为7.3μg/ml;以3μg/ml、6μg/ml、9μg/ml终浓度大蒜素分别作用两种胃癌细胞系24h后,与对照组比较,G0/G1细胞周期百分率明显减少,而G2/M期明显增加(P<0.01);6μg/ml大蒜素作用培养细胞24h后,与对照组比较细胞分裂指数明显增加。提示两种细胞系经大蒜素处理后,细胞周期阻滞于M期;大蒜素与两种抗癌药物联合使用,作用于MGC-803细胞,BLMA5和VCR的24hIC50值分别由单独应用的1.210μg/ml和0.125μg/ml下降到0.370μg/ml和0.031μg/ml,作用于SGC-7901细胞,BLMA5和VCR的24hIC50值分别由单独应用的1.760μg/ml和0.287μg/ml下降到0.680μg/ml和0.074μg/ml,显示低剂量大蒜素增强了抗癌药物对肿瘤细胞的杀伤作用。结论:大蒜素可使MGC-803及SGC-7901两种细胞?

关 键 词:大蒜素  胃癌细胞株  细胞周期  抗癌药物
文章编号:1000-8179(2004)04-0193-04
收稿时间:2003-04-09

Allicin Enhances Cytotoxicity of Antitumor Drugs to Cancer Cells
Ha Minwen, Dong Ming, Wang Lan, . Allicin Enhances Cytotoxicity of Antitumor Drugs to Cancer Cells[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2004, 31(4): 193-196.
Authors:Ha Minwen  Dong Ming  Wang Lan
Affiliation:Cancer Institute, The First Affiliated Hos pital of China Medical University, Shenyang
Abstract:Objective : To study the effect of allicin on human gastric cancer cells lines MGC-803 and SGC-7901 and that combination of allicin with antitumor drugs enhances cytotoxicity of anti-tumor drugs to these cancer cells. Methods : To evaluate the inhibition rates of proliferation of cells bymeans of trypan-blue exclusion, to analyze the change of cell cycle using flow cytometry and Giemsastaining, to study the change of cytotoxicity of BLM A5 and VCR after combination of allicin 3μg/mlwith these cell cycle phase specific antitumor drugs. Results : Allicin inhibited cell growth of MGC-803, IC50 of 24 hours was 6.4μg/ml; Allicin inhibited cell growth of SGC-7901, IC50 of 24 hours was7.3μg/ml. These cells were treated by allicin at the concentrations of 3μg/ml, 6μg/ml, 9μg/ml for 24hours, compared with the control group, the percentage of G0/G1, phase of the cells was decreased andthat of G2/M cells was increased significantly in the allicin treated group (P<0.01). Treated by allicin atthe concentrations of 6μg/ml for 24 hours, compared with the control group, cell division index weremuch higher, it showed that allicin caused arrest of gastricai cancer cells in M phase. In comparisonwith IC50 of BLM A5 and VCR alone or combined with allicin 3μg/ml, the 24h IC50 values decreasedfrom 1.210μg/ml and 0.125μg/ml to 0.370 and 0.031 N.,ml, respectively in MGC-803 cells; and decreased from 1.760μg/ml and 0.287μg/ml to 0.680μg/ml and 0.074μg/ml,respectively in SGC-7901cells. Conclusions : Allicin caused arrest of gastric cancer cells in M phase, and allicin can enhance cy-totoxicity of the cell cycle phase specific antitumor drugs to these cancer cells.
Keywords:Allicin Gastric cancer cells Cell cycle Antitumor drug
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