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目的:探讨Asoprisnil抗小鼠孕卵着床的效果及其对小鼠着床窗期子宫内膜容受性的影响。方法:将孕第1日小鼠随机分成4组,分别为Asoprisnil低(5μg/g)、中(10μg/g)、高(20μg/g)剂量组和对照组,每组22只,于孕第1~3日每日灌胃给药1次,对照组以体积分数1%羧甲基纤维素钠替代,第5日每组处死孕鼠5只取子宫组织,HE染色观察子宫内膜形态学改变,免疫组织化学S-P法检测子宫内膜PCNA表达。第8日处死余下的孕鼠,计数着床点数。结果:①Asoprisnil高、中和低剂量组的妊娠率分别为11.76%、35.29%和76.47%,与对照组(94.12%)比较差异有统计意义(P<0.001)。②Asoprisnil高、中、低剂量组着床胚泡数第50百分位数(P50)分别为13(10.5~14)、10(0.5~11)和0(0~12),与对照组0(0~0)比较差异均有统计学意义(P<0.001)。③对照组围着床期子宫内膜腺体弯曲折叠,为复层高柱状上皮细胞;基质细胞蜕膜变,细胞大且排列疏松,胞质丰富透亮;内膜中腺体和血管丰富。Asoprisnil组子宫内膜腺体为单层或者复层上皮细胞;内膜基质细胞蜕膜变不明显,基质细胞较小,排列致密;腺体和血管增生不明显。④围着床期小鼠子宫内膜腺体和基质中均有PCNA表达。内膜腺体中Asoprisnil高、中、低剂量组PCNA表达强度(AIOD)分别为0.15±0.01、0.16±0.03和0.14±0.02,与对照组(0.21±0.03)比较差异有统计学意义(P<0.001)。Asoprisnil高、中、低剂量组内膜基质细胞中PCNA表达强度(AIOD)分别为0.17±0.01、0.18±0.03和0.17±0.02,与对照组(0.15±0.02)比差异有统计学意义(P<0.001)。结论:Asoprisnil能显著抑制着床窗期子宫内膜腺体增殖,促进子宫内膜基质细胞增殖,但阻止基质细胞蜕膜化,降低子宫内膜容受性而发挥抗小鼠胚胎着床效应,显示出潜在的子宫内膜靶向避孕前景。
OBJECTIVE: To investigate the effect of Asoprisnil on pregnant egg implantation and its effect on endometrial receptivity in mouse window implantation. Methods: The 1st day pregnant mice were randomly divided into 4 groups: Asoprisnil low (5μg / g), medium (10μg / g), high (20μg / g) and control group The rats were intragastrically administrated once daily for 1 ~ 3 days, the control group was replaced by 1% sodium carboxymethylcellulose, and the fifth day, the uterus of 5 pregnant rats were sacrificed. The morphology of endometrium was observed by HE staining Changes in the study, immunohistochemical SP method detection of endometrial PCNA expression. On the 8th day the remaining pregnant rats were sacrificed and the number of implantation sites counted. Results: ① The pregnancy rates of Asoprisnil high, medium and low dose groups were 11.76%, 35.29% and 76.47%, respectively, which were significantly different from those of the control group (94.12%) (P <0.001). (2) The 50th percentile (P50) of implantation blastocyst inAsoprisnil group was 13 (10.5-14), 10 (0.5-11) and 0 (0-12) 0 ~ 0) were statistically significant differences (P <0.001). ③ control group around the implantation of endometrial gland bending fold, stratified high columnar epithelial cells; stromal cells decidua change, large cells and arranged loose, rich and transparent cytoplasm; endometrial glands and rich in blood vessels. Asoprisnil group of endometrial glands as monolayers or stratified epithelial cells; endometrial stromal cells decidua change was not obvious, stromal cells smaller, dense arrangement; glands and vascular proliferation was not obvious. ④ around the implantation mouse endometrial glands and matrix PCNA expression. The expression of PCNA in high, medium and low dose Asprisnil group was 0.15 ± 0.01,0.16 ± 0.03 and 0.14 ± 0.02, respectively, which was significantly lower than that in control group (0.21 ± 0.03) (P < 0.001). The PCNA expression intensity (AIOD) in Asoprisnil high, medium and low dose groups was 0.17 ± 0.01,0.18 ± 0.03 and 0.17 ± 0.02, respectively, which was significantly lower than that in the control group (0.15 ± 0.02) (P < 0.001). CONCLUSION: Asoprisnil can significantly inhibit the proliferation of endometrial glands and promote the proliferation of endometrial stromal cells in bed window, but prevent the stromal cells from decolonization and reduce endometrial receptivity to exert anti-mouse embryo implantation effect. Showing Potential Endometrial Contraceptive Prospects.