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机构地区:[1]浙江中医药大学第一临床医学院,杭州310053 [2]浙江省肿瘤医院中西医结合科,杭州310022
出 处:《浙江中西医结合杂志》2016年第2期105-107,112,202,F0003,共6页Zhejiang Journal of Integrated Traditional Chinese and Western Medicine
摘 要:目的观察川芎嗪(TMP)对乳腺癌MCF7细胞株凋亡的影响及其可能的机制。方法建立乳腺癌MCF7细胞体外培养体系。MTT法检测不同浓度TMP对乳腺癌MCF7细胞增殖的影响,流式细胞仪、电子显微镜和免疫印迹法分别检测各组细胞凋亡比例,观察细胞凋亡特征,检测MAPK信号通路相关基因如ERK、p38和JNK表达水平。结果予0.25、0.50、1.00、1.50、2.00mg/m L TMP处理48h后,MCF7细胞抑制率分别为(2.95±2.45)%、(18.62±4.60)%、(31.15±3.58)%、(47.13±4.15)%和(62.14±5.23)%;0、0.50、1.00、1.50、2.00mg/m L的TMP处理48h,MCF7细胞凋亡率分别为1.58%、3.29%、13.21%、19.23%、29.38%,形态学观察显示典型的凋亡特征。TMP处理后细胞中p-p38和p-JNK蛋白表达以剂量依赖的方式增加,而p-ERK以剂量依赖的方式减少。结论 TMP能诱导乳腺癌MCF7细胞凋亡,其机制可能与激活MAPK信号通路有关。Objective To study the effectof tetramethypyrazine on breast cancer MCF7 Cellapoptosis and the underlying mechanism. Methods Human breast cancer MCF7 cellscultured in vitrowere used to detect the inhibition rate of tetramethypyrazine in different concentrations(0.25, 0.50, 1.00, 1.50, 2.00mg/ml) by MTT assay.The flow cytometry, electron microscope and western blot method were used to detect the apoptosis ratioofdifferent groups; the apoptosis characteristics were observed; andthe level of MAPK signal pathway related genes ERK,p38 and JNK, were determined. Results After treatment with tetramethypyrazine for 48 h, the inhibition rate of human breast cancer MCF7 cells in 0.25, 0.50, 1.00, 1.50, 2.00mg/ml groups were(2.95 ±2.45)%,(18.62 ±4.60)%,(31.15±3.58)%,(47.13±4.15)%, and(62.14±5.23)%, respectively; the apoptosis ratio of MCF7 cells were1.58%,3.29%, 13.21%, 19.23%, and 29.38%. Morphological observation showed typical apoptosis characteristics of MCF7 cells after tetramethypyrazine treatment. The protein expression of p-p38 and p-JNK increased in a dose-dependent manner, but p-ERK reduced. Conclusion Tetramethypyrazinecan induce the apoptosis of breast cancer MCF7 cells, and its mechanism may be related to activation of MAPK signal pathway.
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