缺血性损伤致薄型子宫内膜动物模型的建立

Animal modeling of thin endometrium caused by ischemic injury

目的利用缺血性损伤建立薄型子宫内膜的动物模型。方法将30只SD大鼠分为对照组、模型1组和模型2组各10只。模型1组和2组分别阻断双侧卵巢动脉20 min和30 min,随后恢复血流,对照组不阻断卵巢动脉。5 d后观察各组大鼠子宫内膜组织病理学变化、微血管密度表达、单位内膜面积中波形蛋白及角蛋白的面积。结果与对照组比较,模型1组和2组子宫内膜萎缩变薄(P<0.05),内膜腺体数量减少、排列稀疏且发育迟缓,微血管密度表达较低(P<0.05)、角蛋白及波形蛋白的面积减少(P<0.05)。但模型组间以上指标比较,差异无统计学意义(P>0.05)。结论通过阻断卵巢动脉20 min即可建立"缺血性损伤"薄型子宫内膜动物模型,该方法重复性好,更符合建立简便、快速、最接近人体病理状态动物模型的需求。

Objective To establish the animal model of thin endometrium based on ischemic injury. Methods Thirty SD rats were divided into control group, model Ⅰ group and model Ⅱ group, with 10 rats in each group. The bilateral arteriae ovarica occlusion was performed in the model Ⅰ group and model Ⅱ group for 20 and 30 nlinutes respectively,and then the blood flow reperfused. The arteriae ovarica occlusion was not performed in the control group. After 5 days, the pathological changes of endometrial tissues, expression of endometrial microvessel density（MVD） , areas of vimentin and keratin in unit endometrial areas were observed in three groups. Results Compared to control group, model Ⅰ group and model Ⅱ group had thinner endometrial thickness （ P 〈 0.05 ） , less endometrial glands which appeared sparse arrangement and developmental delay ,lower expression of MVD ,and less areas of vimentin and keratin（ P 〈0. 05 ）. There were no significant differences in the indices mentioned above between two model groups （ P 〉 0.05 ）. Conclusion The ischemic injury-induced animal model of thin endometrium can be established by a 20-ninute arteriae ovarica occlusion. This model has good repeatability, and accorded with the requirement of establishing an animal model simply and rapidly which is more similar to human pathological state.