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作 者:朱夏琴[1] 谭先杰[1] 郎景和[1] 冷金花[1] 朱兰[1] 许秀英[1]
机构地区:[1]中国医学科学院北京协和医院妇产科,北京100730
出 处:《中国实用妇科与产科杂志》2011年第4期280-282,共3页Chinese Journal of Practical Gynecology and Obstetrics
摘 要:目的探讨雌二醇(E2)和孕酮(P4)对体外培养的人子宫内膜基质细胞(ES细胞)血小板反应素-1(TSP-1)表达的影响。方法 2007年12月至2008年10月在北京协和医院用不同浓度的E2及P4处理体外培养的ES细胞一定时间(研究组),提取细胞RNA和蛋白,分别用Northern blot和Western blot方法比较研究组和未用激素刺激的对照组之间TSP-1 mRNA和蛋白水平的差异。结果 E2能抑制ES细胞TSP-1的表达,与对照组相比,用10nmol/L的E2处理ES细胞后,其TSP-1 mRNA和蛋白水平分别下降(47.6±6.5)%(P<0.05)和(49.0±8.6)%(P<0.05);高浓度P4(10μmol/L)能诱导ES细胞表达TSP-1,与对照组相比,10μmol/L的P4处理ES细胞后,其TSP-1 mRNA和蛋白水平分别是对照组的(2.1±0.4)倍(P<0.05)和(2.3±0.6)倍(P<0.05);低浓度(10nmol/L)P4能增强E2对TSP-1蛋白表达的抑制作用,但对其mRNA的表达无明显影响。结论雌激素和孕激素能有差别地调节ES细胞TSP-1的表达,这一发现为子宫内膜异位症的雌激素依赖提供了证据,同时也部分解释了孕激素治疗子宫内膜异位症的机制。Objective To evaluate the effects of estrogen (E2 ) and progesterone (P4) on the expression of thromobospondin-1 (TSP-1) in cultured human endometrial stromal cells (ESCs). Methods ESCs were isolated, cultured in Peking Union medical college hospital between December, 2008 and October 2009. ESCs were treated with different concentrations of E2 and P4 for designed hours, then total RNA and protein were extracted for analysis of TSP-1 expression with Northern blot and Western blot respectively. Results E2 inhbited TSP-1 expression in ESCs. Compared with untreated cells, TSP-1 mRNA and protein levels in ESCs treated with E2 (10nmol/L) were reduced by (47. 6 ±6. 5)% (P 〈 0. 05 )and (49. 0 ±8. 6 )% (P 〈 0. 05 ) respectively. Progesterone at a high concentration (10μmol/L) induced TSP-1 expression. TSP-1 mRNA and protein in ESCs treated with P4(10μmol/L) was as (2. 1 ±0. 4) times(P 〈0. 05) and (2. 3 ±0. 6) times ( P 〈 0. 05 ) higher than those in untreated cells ( P 〈 0. 05 ). P4 at a low concentration ( 10nmol/ L) enhanced the inhibitory effect of E2 on TSP-1 protein but not mRNA expression. Conclusion The findings that estrogen and progesterone differentially regulate the expression of TSP-1 in ESCs not only provide evidence for the estrogen dependence of endometriosis, but also partly explain the mechanisms by which progestins exert their therapeutic activities in endometriosis.
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