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作 者:李明江[1] 李继俊[1] 赵兴波[1] 张梅娟[1] 王伟[1]
机构地区:[1]山东大学山东省立医院妇产科,济南250021
出 处:《中华妇产科杂志》2005年第1期21-24,共4页Chinese Journal of Obstetrics and Gynecology
基 金:山东省自然科学基金资助项目 (Y2 0 0 2C16)
摘 要:目的 观察米非司酮和利洛司酮对体外异位子宫内膜间质细胞增殖及核因子κB(NF κB)表达的影响。方法 取卵巢子宫内膜异位囊肿的异位内膜间质细胞进行体外培养 ,根据不同的药物浓度对内膜间质细胞培养液进行分组 :米非司酮浓度为 1× 10 -6mol/L者 ,为米非司酮Ⅰ组 ,浓度为 1× 10 -5mol/L者 ,为米非司酮Ⅱ组 ;利洛司酮的浓度为 1× 10 -6mol/L者 ,为利洛司酮Ⅰ组 ,浓度为 1× 10 -5mol/L者 ,为利洛司酮Ⅱ组。对照组培养液为 0 5 %乙醇。应用四甲基偶氮唑蓝 (MTT)法检测米非司酮和利洛司酮对内膜间质细胞的抑制作用。应用免疫细胞化学法和原位杂交法 ,检测各组内膜间质细胞NF κBP6 5蛋白和NF κBP6 5mRNA的表达。结果 米非司酮Ⅰ组、米非司酮Ⅱ组、利洛司酮Ⅰ组、利洛司酮Ⅱ组、对照组内膜间质细胞NF κBP6 5蛋白的表达分别为 (6 3 9± 3 5 )分、(49 1± 2 6 )分、(5 6 2± 2 9)分、(35 3± 2 1)分、(78 7± 2 4 )分 ;NF κBP6 5mRNA的表达分别为 (5 7 3± 3 3)分、(43 2± 3 1)分、(48 4± 2 7)分、(2 8 6± 1 8)分、(82 8± 4 6 )分。NF κBP6 5蛋白及NF κBP6 5mRNA的表达强度 ,均为对照组 >米非司酮Ⅰ组、利洛司酮Ⅰ组 >米非司酮Ⅱ组、利洛司酮Ⅱ组 ;米非司酮组Ⅰ、Ⅱ组 >利洛司酮组?Objective To evaluate the effects of antiprogestins mifepristone and lilopristone on proliferation and expressions of nuclear factor kappa B(NF κB) of ectopic stromal cells in vitro Methods The ectopic stromal cells of ovary were cultured in vitro Methyl thiazolyl tetrazolium method was used to evaluate proliferative activity of ectopic stromal cells Cells were divided into five groups according to drug concentration: control group, groupⅠand group Ⅱ of mifepristone and of lilopristone The expressions of NF κB P65 and NF κB P65 mRNA of ectopic stromal cells were determined by immunocytochemistry and in situ hybridization of cell slice Results Antiprogestins mifepristone and lilopristone were able to significantly suppress the proliferation of ectopic stromal cells in a time and dose dependent manner in vitro The expressions of NF κB P65 and NF κB P65 mRNA of ectopic stromal cells in the control group were higher than that of groupⅠand group Ⅱ Their expressions in mifepristone groups were higher than that of lilopristone groups Conclusions Antiprogestin mifepristone and lilopristone could significantly suppress the proliferation of ectopic stromal cells in a time and dose dependent manner in vitro The action mechanisms may be associated with the suppression of expression of NF κB P65 mRNA and NF κB P65
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