【摘要】 目的 探讨自体脂肪间充质干细胞（ADSCs）对宫腔粘连的修复作用及可能涉及的分子生物学机制。方法 取C57BL-6雌性小鼠32只，分为4组，每组8只。假手术组剖腹后缝合，不接受治疗；磷酸盐缓冲液（PBS）模型组剖腹后在子宫壁反复搔刮20次进行建模，关腹后7 d再次开腹，双侧子宫角注射PBS 10μL;ADSCs组于建模7 d后再次开腹，双侧子宫角注射自体ADSCs; ADSCs+3D细胞水凝胶(ShakeGel^TM3D)组于建模7 d后，双侧子宫角注射ADSCs+ShakeGel^TM3D。治疗7 d后处死小鼠，收集双侧子宫，包埋切片后进行H-E和Masson染色，计算子宫内膜厚度、腺体数量和子宫内膜的纤维化面积，评价利用ADSCs和ADSCs+ShakeGel^TM3D治疗宫腔粘连的疗效。结果 ADSCs组和ADSCs+ShakeGel^TM3D组小鼠的子宫内膜厚度和腺体数量明显增加，子宫内膜纤维化面积明显减少，α-平滑肌肌动蛋白（α-SMA）和转化生长因子-β1（TGF-β1）的表达水平降低，骨形态发生蛋白-7（BMP7）和Smad5的表达水平则提高。结论 自体ADSCs和ADSCs+ShakeGel^TM3D可通过BMP7/Smad5通路增加子宫内膜的厚度和腺体的数量，并降低子宫内膜纤维化程度，促进子宫内膜组织修复，恢复其部分功能，起到治疗宫腔粘连的作用。更多还原

【Abstract】 Objective To investigate the repair effect of autologous adipose-derived mesenchymal stem cells（ ADSCs） on intrauterine adhesions and the possible molecular biological mechanisms involved. Methods 32 female C57 BL-6 mice were divided into 4 groups, 8 in each group. The sham operation group was only sutured after laparotomy without treatment; after laparotomy, the mice in the PBS model group were repeatedly scratched 20 times in the uterine wall for modeling, and were reopened 7 days after closure. PBL 10 μL was injected into bilateral uterine horns. The ADSCs group was reopened 7 days after modeling, and autologous ADSCs were injected into bilateral uterine horns; ADSCs + 3D cell hydrogel(ShakeGel^TM3D) group was injected into bilateral uterine horns 7 days after modeling. After 7 days of treatment, the mice were sacrificed, and bilateral uterus were collected. H-E and Masson staining were performed after embedding sections. The thickness of endometrium, the number of glands and the fibrosis area of endometrium were calculated. The efficacy of ADSCs and ADSCs+ShakeGel^TM3D in the treatment of intrauterine adhesions was evaluated. Results The endometrial thickness and the number of glands in the autologous ADSCs and ADSCs+ShakeGel^TM3D treatment groups were significantly increased, the area of endometrial fibrosis was significantly reduced, the expression levels of alpha-smooth muscle actin（α-SMA） and transforming growth factor-beta1（TGF-β1） were decreased, and the expression levels of bone morphogenetic protein-7（BMP7） and Smad5 were increased. Conclusions Autologous ADSCs and ADSCs+ShakeGel^TM3D treatment can reduce the degree of endometrial fibrosis through the BMP7-Smad5 pathway, and promote endometrial tissue repair and partial functional recovery.更多还原