Clinical significance of VEGF, ER and AR expression in seminoma

To evaluate the expression of vascular endothelial growth factor (VEGF), estrogen receptor (ER) and androgen receptor (AR) in the genesis and development of seminoma. Methods: The expression of VEGF, ER and AR was assayed by means of immuno-histochemical technique in 16 cases of seminoma and 10 cases of prostatic cancer (Pca). Results: The VEGF expression positive rate was significantly higher (P<0.05) in seminoma than in Pca, being 14/16(87.5 %) and (4/10, 40%), respectively. The AR expression positive rate was lower (P>0.05) in seminoma (9/16, 56.2%) than in Pca (9/10, 90%). The ER expression was negative in all the seminoma and Pca patients. Conclusion: In seminoma, the expression of VEGF is significantly increased, which may play a role in the genesis and development of the neoplasm. (Chin J Androl 2002; 16: 349)     

Expression of N-acetyl-glucosamine-6-O-sulfotransferase in the endometrium of implantation window stage from infertile patients

Objective:To observe the expression of N-acetyl-glucosamine-6-O-sulfotransferase(GN-6-ST)in the endometrium during the window stage of implantation from infertile women before IVF-ET treatment,we compared the GN-6-ST gene expression level between the women with succeeded and failed implantation,and investigated the roles of selectin and its ligands in the embryo implantation.Methods:The hysteroscopy and endometrial biopsies were performed in patients prior to undergoing IVF-ET treatment in the IVF Center of the First Affiliated Hospital of Nanjing Medical University from July 2004 to March 2005.Fourteen patients who succeeded in implantation were taken as study group,while the 28 infertile patients with failed implantation served as control group.The RT-PCR method was used to detect the mRNA levels of N-acetyl-glucosamine-6-O-sulfotransferase in the endometrium during the window stage of imp-lantation of the women from both groups.Results:For these infertile patients with succeeded implantation,the average mRNA expression level of acetyl-glucosamine-6-O-sulfotransferase in the endometrium during the window stage of implantation was(0.65±0.33),while for those with failed implantation cycle,the average mRNA expression level was(0.41±0.36),which was significantly lower than that of study group,P<0.05.Conclusions:The combination of the selectin and ligands may play a role in the embryo implantation capacibility.     

Expression and significance of estrogen receptor α and β in prostate cancer and peri-cancer tissue

Objective To investigate the expression of estrogen receptor (ER) α and β in human prostate cancer (PC), peri-cancer tissue and benign prostatic hyperplasia (BPH) tissue, and to discuss the role of estrogen receptor in prostate cancer. Methods The expression of ERα and ERβ in PC (n=28), peri-cancer tissue (n=28) and BPH (n=29) were detected by immunohistochemistry with En vision method. The ERα and ERβ expression were compared among different tissues by chisquare. The relationship between ER expression and related clinicopathologic features was statistically analyzed by spearman rank collection. Results ERα was localized dominantly in the stromal cell of PC. There were significant differences of the expression of ERα in PC, peri-cancer tissue and BPH tissue (epithelial cell 0%, 14%, 24%, P＜0. 05; stromal cell 57%, 68%, 31%,P＜0. 05). ERβ was localized in both epithelial and stromal cell of PC. There were significant differences of the expression of ERβ in PC, peri-cancer tissue and BPH tissue (epithelial cell 39%, 64%, 29%, P＜0.01; stromal cell 50%, 75%, 79%, P＜0.05). There was a significant difference of the expression of ERβ in different Gleason scores of PC tissue. Conclusions ERα is localized in the stromal cell of PC tissue.ERβ is localized in both epithelial and stromal cell of PC tissue. The ERβ might be related to the tumor differentiation of PC.     

Expression and significance of estrogen receptor α and β in prostate cancer and peri-cancer tissue

Objective To investigate the expression of estrogen receptor (ER) α and β in human prostate cancer (PC), peri-cancer tissue and benign prostatic hyperplasia (BPH) tissue, and to discuss the role of estrogen receptor in prostate cancer. Methods The expression of ERα and ERβ in PC (n=28), peri-cancer tissue (n=28) and BPH (n=29) were detected by immunohistochemistry with En vision method. The ERα and ERβ expression were compared among different tissues by chisquare. The relationship between ER expression and related clinicopathologic features was statistically analyzed by spearman rank collection. Results ERα was localized dominantly in the stromal cell of PC. There were significant differences of the expression of ERα in PC, peri-cancer tissue and BPH tissue (epithelial cell 0%, 14%, 24%, P＜0. 05; stromal cell 57%, 68%, 31%,P＜0. 05). ERβ was localized in both epithelial and stromal cell of PC. There were significant differences of the expression of ERβ in PC, peri-cancer tissue and BPH tissue (epithelial cell 39%, 64%, 29%, P＜0.01; stromal cell 50%, 75%, 79%, P＜0.05). There was a significant difference of the expression of ERβ in different Gleason scores of PC tissue. Conclusions ERα is localized in the stromal cell of PC tissue.ERβ is localized in both epithelial and stromal cell of PC tissue. The ERβ might be related to the tumor differentiation of PC.     

Expression of vascular endothelial growth factor and its two receptors in normal human endometrium

<正> Objectives:We try to demonstrate the expression of vascular endothelial growthfactor (VEGF) and its receptors,flt-1 and KDR,in normal human emdometrium duringthe menstrual cycle.Methods:Immunohistochemical method was used to observe the expression ofVEGF and its two receptors in emdometrium throughout the normal menstrual cyclemeanwhile the isoforms of VEGF were also detected by Western blot analysis.The en-dothelial cells of micro-vessels were marked with VIII factor antibody.Results:VEGF and its receptors existed in endometrial glandular,stromal and vas-cular endothelial cells of human endometrium.Their expressions were higher in the mid-secretory phase of menstrual cycle and highest at menstruation.VEGF_(121) and VEGF_(165)were the predominant isoforms in normal human endometrium.Conclusion:The expression of VEGF and its two receptors showed cycle-dependentin human endometrium,probably involved in embryonic implantation and endometrialproliferation and differentiation.     

Inhibitory effect of vascular endothelial growth factor on transforming growth factor β1-induced epithelial-mesenchymal transition of HK2 cells and its relationship with connective tissue growth factor and PI3K-Akt pathway

Objective To examine the relationship of the inhibitory effect of vascular endothelial growth factor(VEGF) on epithelial-mesenchymal transition (EMT) induced by TGF-β1 in HK2 cells with the expression of connective tissue growth factor (CTGF) and PI3K-Akt pathway. Methods The cultured HK2 cells were divided into the following groups: normal control group, TGF-β1 (5 μg/L) group, VEGF (100 μg/L) group, TGF-β1 plus VEGF group. LY294002 (25 μmol/L), the blocker of PI3K-Akt pathway, was added to each of above-mentioned groups for the second part of the study, α-smooth muscle actin (α-SMA) and E-cadherin expressions of HK2 cells were assessed with double-stain immunocytochemistry method. The mRNA and protein expressions of α-SMA and CTGF of cells were assessed with RT-PCR and Western blot. The expressions of fibronectin (FN) and collagen Ⅰ (Col Ⅰ) in medium were assessed with ELISA. Results The expressions of α-SMA and CTGF significantly increased in HK2 cells treated with TGF-β1 compared with those in normal control (P<0.05), while significantly decreased in cells co-treated with TGF-β1 and VEGF compared with those treated with TGF-β1 alone (P<0.05, respectively). The expression of E-cadherin was exactly opposite to that of α-SMA. When LY294002 was added to TGF-β1 and VEGF co-treated cells, the expressions of α-SMA, CTGF, FN and Col Ⅰ were markedly up-regulated, when compared with those without LY294002 treatment (P<0.05). Conclusion Inhibitory effect of VEGF on TGF-β1-induced EMT of HK2 ceils in vitro may be related to down-regulation of CTGF expression and reduction of FN and Col Ⅰ, which may be partly dependent on PI3K-Akt pathway.     

Inhibitory effect of vascular endothelial growth factor on transforming growth factor β1-induced epithelial-mesenchymal transition of HK2 cells and its relationship with connective tissue growth factor and PI3K-Akt pathway

Objective To examine the relationship of the inhibitory effect of vascular endothelial growth factor(VEGF) on epithelial-mesenchymal transition (EMT) induced by TGF-β1 in HK2 cells with the expression of connective tissue growth factor (CTGF) and PI3K-Akt pathway. Methods The cultured HK2 cells were divided into the following groups: normal control group, TGF-β1 (5 μg/L) group, VEGF (100 μg/L) group, TGF-β1 plus VEGF group. LY294002 (25 μmol/L), the blocker of PI3K-Akt pathway, was added to each of above-mentioned groups for the second part of the study, α-smooth muscle actin (α-SMA) and E-cadherin expressions of HK2 cells were assessed with double-stain immunocytochemistry method. The mRNA and protein expressions of α-SMA and CTGF of cells were assessed with RT-PCR and Western blot. The expressions of fibronectin (FN) and collagen Ⅰ (Col Ⅰ) in medium were assessed with ELISA. Results The expressions of α-SMA and CTGF significantly increased in HK2 cells treated with TGF-β1 compared with those in normal control (P<0.05), while significantly decreased in cells co-treated with TGF-β1 and VEGF compared with those treated with TGF-β1 alone (P<0.05, respectively). The expression of E-cadherin was exactly opposite to that of α-SMA. When LY294002 was added to TGF-β1 and VEGF co-treated cells, the expressions of α-SMA, CTGF, FN and Col Ⅰ were markedly up-regulated, when compared with those without LY294002 treatment (P<0.05). Conclusion Inhibitory effect of VEGF on TGF-β1-induced EMT of HK2 ceils in vitro may be related to down-regulation of CTGF expression and reduction of FN and Col Ⅰ, which may be partly dependent on PI3K-Akt pathway.     

Inhibitory effect of vascular endothelial growth factor on transforming growth factor β1-induced epithelial-mesenchymal transition of HK2 cells and its relationship with connective tissue growth factor and PI3K-Akt pathway

Objective To examine the relationship of the inhibitory effect of vascular endothelial growth factor(VEGF) on epithelial-mesenchymal transition (EMT) induced by TGF-β1 in HK2 cells with the expression of connective tissue growth factor (CTGF) and PI3K-Akt pathway. Methods The cultured HK2 cells were divided into the following groups: normal control group, TGF-β1 (5 μg/L) group, VEGF (100 μg/L) group, TGF-β1 plus VEGF group. LY294002 (25 μmol/L), the blocker of PI3K-Akt pathway, was added to each of above-mentioned groups for the second part of the study, α-smooth muscle actin (α-SMA) and E-cadherin expressions of HK2 cells were assessed with double-stain immunocytochemistry method. The mRNA and protein expressions of α-SMA and CTGF of cells were assessed with RT-PCR and Western blot. The expressions of fibronectin (FN) and collagen Ⅰ (Col Ⅰ) in medium were assessed with ELISA. Results The expressions of α-SMA and CTGF significantly increased in HK2 cells treated with TGF-β1 compared with those in normal control (P<0.05), while significantly decreased in cells co-treated with TGF-β1 and VEGF compared with those treated with TGF-β1 alone (P<0.05, respectively). The expression of E-cadherin was exactly opposite to that of α-SMA. When LY294002 was added to TGF-β1 and VEGF co-treated cells, the expressions of α-SMA, CTGF, FN and Col Ⅰ were markedly up-regulated, when compared with those without LY294002 treatment (P<0.05). Conclusion Inhibitory effect of VEGF on TGF-β1-induced EMT of HK2 ceils in vitro may be related to down-regulation of CTGF expression and reduction of FN and Col Ⅰ, which may be partly dependent on PI3K-Akt pathway.     

Inhibitory effect of vascular endothelial growth factor on transforming growth factor β1-induced epithelial-mesenchymal transition of HK2 cells and its relationship with connective tissue growth factor and PI3K-Akt pathway

Objective To examine the relationship of the inhibitory effect of vascular endothelial growth factor(VEGF) on epithelial-mesenchymal transition (EMT) induced by TGF-β1 in HK2 cells with the expression of connective tissue growth factor (CTGF) and PI3K-Akt pathway. Methods The cultured HK2 cells were divided into the following groups: normal control group, TGF-β1 (5 μg/L) group, VEGF (100 μg/L) group, TGF-β1 plus VEGF group. LY294002 (25 μmol/L), the blocker of PI3K-Akt pathway, was added to each of above-mentioned groups for the second part of the study, α-smooth muscle actin (α-SMA) and E-cadherin expressions of HK2 cells were assessed with double-stain immunocytochemistry method. The mRNA and protein expressions of α-SMA and CTGF of cells were assessed with RT-PCR and Western blot. The expressions of fibronectin (FN) and collagen Ⅰ (Col Ⅰ) in medium were assessed with ELISA. Results The expressions of α-SMA and CTGF significantly increased in HK2 cells treated with TGF-β1 compared with those in normal control (P<0.05), while significantly decreased in cells co-treated with TGF-β1 and VEGF compared with those treated with TGF-β1 alone (P<0.05, respectively). The expression of E-cadherin was exactly opposite to that of α-SMA. When LY294002 was added to TGF-β1 and VEGF co-treated cells, the expressions of α-SMA, CTGF, FN and Col Ⅰ were markedly up-regulated, when compared with those without LY294002 treatment (P<0.05). Conclusion Inhibitory effect of VEGF on TGF-β1-induced EMT of HK2 ceils in vitro may be related to down-regulation of CTGF expression and reduction of FN and Col Ⅰ, which may be partly dependent on PI3K-Akt pathway.     

“河车助孕方”对不育症子宫内膜雌激素受体、孕激素受体、增殖细胞核抗原及血管内皮生长因子的影响

目的 :探讨补肾调经中药治疗不育症的机理。方法 :应用免疫组织化学方法 ,观察服用“河车助孕方”前、后增殖晚期子宫内膜雌激素受体 (ER)、孕激素受体 (PR)、增殖细胞核抗原 (PCNA)及血管内皮生长因子 (VEGF )表达的变化 ,并以服药前作为自身对照。结果 :服药前 ER、PR、PCNA、VEGF在子宫内膜腺上皮细胞核的表达分别为 0 .18± 0 .3 9、0 .88± 0 .3 8、1.76± 0 .5 0、0 .15± 0 .2 9;在内膜间质细胞核的表达分别为 0 .71±0 .44、0 .79± 0 .47、1.12± 0 .47、0 .2 6± 0 .3 6;服药后在子宫内膜腺上皮细胞核的上述各项表达分别为 2 .12± 0 .40、2 .3 2± 0 .3 5、3 .15± 0 .49、1.79± 0 .44 ,与服药前比较 ,P均 <0 .0 0 1;在内膜间质细胞核的表达分别为 1.5 3± 0 .41、1.88± 0 .3 8、2 .18± 0 .5 0、2 .0 6±0 .3 9,与服药前比较 ,P均 <0 .0 0 1;服药后子宫内膜腺上皮细胞、间质细胞的 PCNA、VEGF表达亦明显增强。结论 :补肾调经中药“河车助孕方”可增加子宫内膜 ER、PR的合成 ,并使激素依赖性的 PCNA、VEGF表达增强 ,从而促进内膜正常生长、发育 ,有效地改善不育症患者子宫内膜的微环境。     

左炔诺孕酮宫内节育系统治疗无排卵型功能失调性子宫出血的疗效

目的观察左炔诺孕酮宫内节育系统(曼月乐,LNG-IUS)治疗无排卵型功能失调性子宫出血(AUB-O)的疗效及其对子宫内膜血管内皮细胞生长因子、雌激素受体和孕激素受体的影响。方法将2015年6月~2016年9月我院收治的78例AUB-O患者,随机分为对照组和观察组,每组39例。在常规治疗基础上,对照组予去氧孕烯炔雌醇片(妈富隆)口服,观察组予曼月乐治疗。比较两组治疗前与治疗12个月后血红蛋白水平(HGB)、血清雌二醇(E_2)、孕酮(P)、垂体分泌卵泡刺激素(FSH)、黄体生成素(LH)激素水平及子宫内膜厚度,采用SP免疫组织化学检测两组治疗前及12个月后子宫内膜腺体和间质中的血管内皮生长因子(VEGF)、雌激素受体(ER)、孕激素受体(PR)的阳性表达。比较两组的临床疗效、不良反应。结果观察组的控制出血及完全止血时间均显著短于对照组,差异均有统计学意义(P0.01)。治疗后,两组的血红蛋白水平均较治疗前显著升高(P0.01),子宫内膜厚度显著减少(P0.01),E_2均较治疗前显著降低,P显著升高,且观察组改善程度较对照组更加明显,差异亦有统计学意义(P0.01)。观察组患者治疗后的子宫内膜腺体及间质中的VEGF阳性率显著高于治疗前,ER、PR阳性率显著低于治疗前(P0.01)。且治疗后观察组的VEGF阳性率高于对照组,ER、PR阳性率低于对照组(P0.01)。观察组的的总有效率为94.9%,显著高于对照组的79.5%(P0.05)。两组的不良反应发生情况无统计学差异(P0.05)。结论曼月乐治疗AUB-O能更好的通过调节子宫内膜ER、PR、VEGF的表达,达到临床治疗效果,且较口服妈富隆更加简便、有效、安全。     

无排卵性功能失调性子宫出血患者子宫内膜雌、孕激素受体及基质金属蛋白酶表达变化的研究

目的研究无排卵性功能失调性子宫出血(功血)患者子宫内膜雌激素受体(ER)、孕激素受体(PR)、IV型胶原、基质金属蛋白酶-9(MMP-9)及其抑制物-1(TIMP-1)的表达,探讨无排卵性功血的发病机制。方法采用免疫组化法检测20例正常增殖期子宫内膜(对照组)和66例无排卵性功血患者(病例组)子宫内膜腺上皮和基质细胞ER、PR、IV型胶原、MMP-9及TIMP-1表达。结果病例组子宫内膜腺上皮和基质ER、PR表达高于对照组(P<0.05),MMP-9水平明显增加(P<0.05),MMP-9/TIMP-1比值升高(P<0.01),IV型胶原含量明显下降(P<0.01)。相关分析显示,无排卵性功血患者子宫内膜MMP-9水平与ER、PR均呈正相关(r=0.605,P<0.05;r=0.697,P<0.05)。结论无排卵性功血患者子宫内膜出血原因可能与雌激素作用下ER、PR表达失调有关,且MMP-9水平异常升高,导致细胞外基质过度降解,临床表现为子宫不规则出血。     

子宫内膜息肉中雌、孕激素受体的表达

目的检测子宫内膜息肉雌激素受体(ER)、孕激素受体(PR)的表达,探索子宫内膜息肉形成的原因及机制。方法子宫内膜息肉48例为观察组,正常子宫内膜36例为对照组,采用免疫组化SP法,行半定量分析,检测ER、PR的表达。结果增殖期的息肉组织中PR表达的评分结果为(2.89±2.16),低于增殖内膜的评分(4.04±1.73),差异有统计学意义(P<0.05);分泌期的内膜息肉中ER表达的评分结果为(3.80±1.64),高于分泌期内膜中的评分(2.64±1.45),差异有统计学意义(P<0.05)。结论增殖期的子宫内膜息肉中PR的表达降低及分泌期的息肉中ER表达增高可能参与了子宫内膜息肉的形成及发展。     

生长抑素受体和雌激素受体在原发性乳腺癌中的表达及其意义

目的研究生长抑素受体(SSTR)与雌激素受体(ER)、孕激素受体(PR)在原发性乳腺癌中的表达及其意义。方法 采用免疫组织化学链霉菌抗生物素蛋白-过氧化酶(SP)法检测SSTR和ER、PR在68例乳腺癌中的表达。结果 在68例乳腺癌中,SSTR阳性表达44例(64.70％),ER、PR阳性表达51例(75.70％),ER、PR和SSTR同时阳性表达阳性41例(60.29％)。ER、PR和SSTR两者表达呈正相关(r=0.651 6,P<0.05)。SSTR阳性患者复发率和死亡率低于SSTR阴性者(P<0.05);SSTR阳性且ER、PR阳性患者复发率和死亡率明显低于SSTR阴性ER、PR阴性患者(P<0.01)。病理分化低的有47例,SSTR阳性表达36例(P>0.05)。结论SSTR表达与ER、PR表达有明显相关性,有可能作为判断乳腺癌预后的指标。     

米非司酮对人蜕膜中雌激素及孕酮受体的影响

本研究观察了服用米非司酮后人蜕膜中雌激素受体（ＥＲ）和孕酮受体（ＰＲ）的变化。６０名孕６～７周的妇女，被随机分为３组。在手术终止妊娠前的１２和２４小时两组中，分别一次性口服米非司酮２００ｍｇ，对照组服用安慰剂。服用米非司酮后，蜕膜中ＥＲ和ＰＲ的免疫组织化学染色反应与对照组比较增强了。卡方分析表明，服用米非司酮后，ＥＲ阳性标本的数量明显增加     

HOXA11在人子宫内膜和早孕蜕膜中的表达及与不育的关系

目的检测HOXA11蛋白在正常月经周期子宫内膜、早孕蜕膜和不明原因不育子宫内膜组织中的表达,探讨HOXA11与不明原因不育及雌孕激素受体(ER、PR)表达的相关性。方法采用免疫组织化学和Western-Blot方法对38例正常子宫内膜、15例早孕蜕膜和19例不明原因不育子宫内膜组织中HOXA11、ER及PR的表达。结果HOXA11蛋白在子宫内膜腺上皮和基质细胞均有表达,以分泌中晚期子宫内膜和早孕蜕膜表达量较高;在不育内膜的表达量显著降低(P<0.05);ER、PR在各组表达量的变化与HOXA11相同,即分泌中晚期子宫内膜和早孕蜕膜的表达量较高,而在不育内膜的表达量显著下降(P<0.05)。结论HOXA11基因在着床期子宫内膜的分化、发育以及着床后妊娠的维持起一定作用;HOXA11表达量下降与ER、PR表达量降低相关;HOXA11表达下降或缺失可能是女性不明原因不育的原因之一。     

乳腺癌组织中ERβmRNA和VEGFmRNA的表达及两者的关系

目的：探讨雌激素受体亚型β（ERβ）和血管内皮细胞生长因子（VEGF）在乳腺癌组织中的表达及两者之间的关系。方法：采用半定量逆转录聚合酶链式反应（RT PCR）检测35例乳腺癌组织中ERβmRNA和VEGFmRNA的表达，分析两者表达的相关性及其与肿瘤病理参数的关系。结果：ERβmRNA表达水平与VEGF121和VEGF165mRNA的表达水平呈正相关（r=0.785和0.641，均P=0.000）。VEGF121和VEGF 165mRNA在有淋巴结转移的乳腺癌组织中表达水平明显高于无淋巴结转移者（P=0.033，0.004）。结论：乳腺肿瘤血管生成可能受ERβ的影响，而乳腺癌组织中VEGFmRNA的表达水平高者可能易于发生淋巴结转移。     

Understanding the biologic mechanisms responsible for breast-cancer progression during tamoxifen or fulvestrant treatment

BACKGROUND: Dehydroepiandosterone sulfate (DHEAS) causes breast-cancer proliferation, even during tamoxifen or fulvestrant blockade. The purpose of this study was to determine possible mechanisms for this treatment failure. METHODS: T-47D cells (estrogen receptor [ER] and progesterone receptor [PR] positive) were treated with fulvestrant (10 micromol/L), tamoxifen (10 mmol/L or 0.0001 nmol/L), or vehicle and stimulated with DHEAS. Gene expression of ER, PR, insulin-like growth factor (IGF)-1 and -2, and insulin-like growth-factor binding protein (IGFBP)-1 through -4 was determined. RESULTS: ER and PR gene expression decreased by 1.3- and 4-fold with fulvestrant and DHEAS. ER expression decreased by 2.7-fold with 0.0001 nmol/L tamoxifen and DHEAS. ER and PR expression were unchanged by 10 nmol/L tamoxifen. IGF-1 and IGF-2 were not expressed. IGFBP-2 and -4 expression decreased by 1.9- and 1.6-fold after DHEAS stimulus, although this was not statistically significant. CONCLUSIONS: DHEAS exposure, even in the presence of tamoxifen and fulvestrant, induces changes in ER and PR gene expression that may be partially responsible for breast cancer progression.     

米非司酮对子宫内膜整合素亚单位α4和β3表达的影响

为探讨米非司酮对与子宫内膜接受性建立相关的整合素的影响。对 1 9例正常生育妇女进行两个连续月经周期的前瞻性、自身对照研究。应用免疫组织化学方法检测口服米非司酮前后种植窗期子宫内膜整合素亚单位α 4(1 9例 )和β 3 (9例 )、以及孕激素受体 (PR,1 9例 )表达的情况 ,应用 HSCORE评分作半定量分析 ,用非参数 Wilcoxon检验作统计学处理。结果 :种植窗期正常子宫内膜腺体及血管内皮表达整合素亚单位 α4和β3 ;黄体中期服用米非司酮 5 0 mg,明显降低整合素亚单位 α4和 β3、以及 PR在子宫内膜腺体的表达。提示损害子宫内膜接受性是米非司酮用于紧急避孕的机制之一 ;整合素亚单位 α4和 β3在子宫内膜腺体的表达受孕激素的调节。米非司酮降低整合素亚单位 α4和 β3在子宫内膜腺体的表达可能与其降低腺体 PR的表达有关