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作 者:刘家仁[1] 杨艳梅[1] 董宏伟[1] 孙向荣[1] 于佳[1] 赵淑媛[1] 陈炳卿[1]
机构地区:[1]哈尔滨医科大学公共卫生学院,哈尔滨150086
出 处:《卫生研究》2005年第6期706-709,共4页Journal of Hygiene Research
基 金:国家自然科学基金资助项目(No.30200229)
摘 要:目的为了研究β紫罗兰酮对雌激素受体阴性的人乳腺癌细胞(MDAMB435)MAPKs途径的影响。方法采用细胞生长曲线,细胞核分裂,集落形成以及DNA合成试验,Westernblotting方法,观察了用不同浓度β紫罗兰酮(25、50、100和200μmolL)对MDAMB435细胞生长的影响及其对细胞增殖相关蛋白如PCNA和MAPKs途径的作用。结果β紫罗兰酮可明显抑制MDAMB435细胞生长,细胞核分裂,集落形成和DNA合成。7天的抑制率分别为45.65%,71.24%,81.53%和84.93%;IC50值为42.0μmolL。细胞核分裂的抑制率24小时为-34.57%~58.857%,48小时为-30.05%~75.12%;集落形成试验的抑制率24小时为4.44%~63.79%,48小时为6.42%~95.55%;DNA合成抑制率24h为17.00%~57.56%,48h为62.25%~78.35%。采用Westernblotting方法进一步对其抑制机制结果表明,β紫罗兰酮可抑制PCNA蛋白的表达,抑制MAPK途径中的ERK和MEK1的表达,促进JNK和MKP1的表达。结论β紫罗兰酮对MDAMB435细胞有明显地抑制作用;β紫罗兰酮影响MAPKs级联反应可能是其抑制肿瘤作用的机制之一。Objective To investigate the effect of cell proliferation in human breast cancer cells ( MDA-MB 435 ), which has non-receptor of estrogen (Er^-), induced by β-ionone. MDA-MB 435 cells were treated with different β-ionone concentrations (25, 50, 100 and 200μmol/L) , with a negative control. Methods Such as curve of cell growth, cellular mitosis, the clone formatting, DNA synthesis, and western blotting for protein of PCNA and MAPK pathway were employed. Results β-ionone inhibited the cell proliferation, cellular mitosis, clone formatting and DNA synthesis and reduced expression of PCNA protein in MDA-MB 435 cells. The inhibitory frequency (IF) showed a dose-dependent responses as the concentrations of β-ionone increased. Seven days after treatment with various concentrations of β-ionone, as mentioned above, the inhibition rates were 45.65% , 71.24% , 81.53% , and 84.93% , respectively. Its IC50 value was 42.0μmol/L for MDA-MB 435 cells. The IF from cellular mitosis of MDA-MB 435 cells treated by β-ionone were - 34.57% - 58.857% at 24 h and - 30.05% - 75.12% at 48h, from the clone formatting assay, - 4.44% - 63.79% at 24h and 6.42% - 95.55% at 48h, from DNA synthesis, 17.00% - 57.56% at 24h and 62.25% - 78.35% at 48h. The further study was found that β-ionone inhibited the expression of PCNA which to be related to cell cycle and reduced ERK, MEK-1 proteins expression and promoted the expression of JNK and MKP-1 proteins related to MAPK pathway in MDA-MB 435 cells. Conclusion β-ionone could inhibit MDA-MB 435 cells proliferation by regulating MAPKs pathway. It may be one of the effects of β-ionone in anticancer.
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