Chen Xing, Sun Jingtao, Li Xiaoyu, Mao Lele, Zhou Yingfang, Cui Lei, Bai Wenpei
From the Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Exp Clin Transplant. 2019 Apr;17(2):236-242. doi: 10.6002/ect.2017.0284. Epub 2018 Sep 25.
Intrauterine adhesion is a disease involving endometrial fibrosis that arises from injury to the basal layer of the endometrium. Here, we aimed to explore the preventive effects of decellularized and lyophilized amniotic membrane on endometrial fibrosis in a rat model of intrauterine adhesion.
Twenty-four Sprague-Dawley rats were randomly divided into 2 groups. For the intrauterine adhesion group, endometria of left uteri were scraped without treatment. For the intrauterine adhesion plus decellularized and lyophilized amniotic membrane transplant group, decellularized and lyophilized amniotic membrane was sutured onto the scraped wound of left uteri. Right uteri were kept as the control group. At 3, 7, 14, and 28 days after transplant, uteri were sampled for histologic and immunohistochemical evaluation.
Histology examination revealed extensive fibrosis with significantly reduced numbers of endometrial glands in uteri in the intrauterine adhesion group. Immunohistochemical staining showed a remarked increase in expression of transforming growth factor β1 (P < .01) and decreased expression of matrix metalloproteinase-9 (P < .01) in the intrauterine adhesion group. In rats with transplant of decellularized and lyophilized amniotic membrane, endometrial fibrosis apparently improved (P < .05) with reduced expression of transforming growth factor β1 and increased matrix metalloproteinase-9 expression (P < .05). However, there were no significant differences in the number of endometrial glands or endometrial thickness between the 2 groups (P > .05).
Development of intrauterine adhesion was prevented with transplant of decellularized and lyophilized amniotic membrane via suppression of transforming growth factor β1 and increased production of matrix metalloproteinase-9 in a rat model.
宫腔粘连是一种由子宫内膜基底层损伤引起的子宫内膜纤维化疾病。在此，我们旨在探讨脱细胞冻干羊膜对宫腔粘连大鼠模型子宫内膜纤维化的预防作用。
将24只Sprague-Dawley大鼠随机分为2组。宫腔粘连组，左子宫内膜刮除后未进行处理。宫腔粘连加脱细胞冻干羊膜移植组，将脱细胞冻干羊膜缝合到左子宫刮伤处。右子宫作为对照组。移植后3、7、14和28天，取子宫进行组织学和免疫组织化学评估。
组织学检查显示，宫腔粘连组子宫出现广泛纤维化，子宫内膜腺体数量显著减少。免疫组织化学染色显示，宫腔粘连组转化生长因子β1表达显著增加（P <.01），基质金属蛋白酶-9表达降低（P <.01）。在接受脱细胞冻干羊膜移植的大鼠中，子宫内膜纤维化明显改善（P <.05），转化生长因子β1表达降低，基质金属蛋白酶-9表达增加（P <.05）。然而，两组之间子宫内膜腺体数量或子宫内膜厚度无显著差异（P >.05）。
在大鼠模型中，通过抑制转化生长因子β1和增加基质金属蛋白酶-9的产生，脱细胞冻干羊膜移植可预防宫腔粘连的发生。
