绿原酸对MCF-7细胞增殖的影响及机制探讨

目的为绿原酸（CGA）用于乳腺癌的治疗提供依据。方法将不同浓度的CGA干预乳腺癌MCF-7细胞；采用四甲基偶氮唑蓝（MTT）法检测CGA对MCF-7细胞的生长抑制率，流式细胞术检测MCF-7细胞凋亡率、细胞周期及细胞周期素（Cydin）D1表达。结果0．25、0．5mg／mlCGA作用MCF-7细胞48h后，使细胞阻滞于G1／G0期，两组的G1／G0期细胞较对照组明显增加（P〈0．01）；0、0．25、0．5mg／mlCGA处理MCF-7细胞48h后，Cyc-linD1的平均荧光强度比（MFIR）分别为9．64±0．18、9．15±0．22、8．104-0．28（P=0．001）。结论CGA可抑制MCF-7细胞增殖，使细胞阻滞于G0／G1期；其机制可能与下调CyclinD1表达有关。

Effects of chlorogenic acid on cell proliferation of MCF-7 cell and its mechanism

Objective To provide basis for the treatment of breast cancer by ehlorogenie acid （CGA）. Methods The breast cancer cell MCF-7 were treated with different concentrations of CGA ; the effects of CGA on the growth of MCF- 7 cells were studied by MTr assay ,the cell apoptosis, cell cycle and the expression of Cyclin Dlwere analyzed by flow ey- tometry. Results After treated with 0.25,0.5 mg/ml CGA for 48 hs, the cell cycle was arrested at G1/G0phase, the pro- portion of MCF-7 ceils at G1 phase of CGA group increased significantly compared to the control group（ P 〈 0.01 ） ; the mean fluorescence intensity ratio （MFIR） of Cyelin D1 was 9.64 ±0.18,9.15 ± 0.22,8.10± 0.28 （P = 0. 001 ） after the treatment of 0,0.25,0.5 mg/ml CGA. Conclusions CGA can inhibit the proliferation of MCF-7 ceils and induce Gl phase arrest in the cells;the mechanism possibly was down-regulating the expression of Cyelin D1.