中国老年保健医学2026，Vol.24Issue(1)：51-58,8.DOI:10.3969/j.issn.1672-2671.2026.01.009
机械损伤导致宫腔粘连的病理学研究
Pathological study of intrauterine adhesions caused by mechanical injury
摘要
Abstract
Objective To investigate the pathological changes in the endometrium after mechanical injury,focusing on alterations in tissue morphology,physiological function,fibrotic progression,and inflammatory responses,and to clarify the mechanisms underly-ing intrauterine adhesion(IUA)development.Methods Forty-two female C57BL/6 mice were included and randomly assigned to a control group(n=6)and an IUA model group(n=36).In the model group,the endometrium was mechanically scraped with a blunt No.7 needle until uterine congestion and surface roughness were observed.In the control group,the uterus was surgically ex-posed and closed without endometrial injury.Uterine tissues were collected at multiple postoperative time points.Hematoxylin and eo-sin staining was used to assess endometrial thickness and gland count.Immunohistochemistry,Western blotting,and quantitative real-time PCR were performed to evaluate the expression of proliferation marker Ki-67,angiogenesis-related markers CD31 and VEGF,en-dometrial receptivity factor LIF,inflammatory factors,and fibrosis markers including fibronectin,α-smooth muscle actin,and collagen I.Masson staining was applied to assess collagen fiber deposition.Results Multi-time-point analysis demonstrated that endometrial parameters in mice exhibited distinct dynamic changes after mechanical injury.Morphologically,endometrial thickness transiently in-creased during the early phase(Days 1-3),then gradually thinned and stabilized.Functionally,expression of the proliferation marker Ki-67 progressively decreased post-surgery,reaching its lowest level on Day 10.The endometrial receptivity marker leukemia inhibito-ry factor(LIF)showed marked fluctuations and ultimately remained lower than in the control group.Regarding fibrosis,collagen fiber deposition gradually increased over time.Fibronectin(FN)expression remained persistently elevated,while collagen type I(COL1A1)and α-smooth muscle actin(α-SMA)showed an increasing trend.Among inflammatory indicators,the pro-inflammatory cytokine interleukin-6(IL-6)was significantly upregulated after injury.Most of these changes were statistically significant(P<0.05).Conclusion Mechanical injury can induce a sustained inflammatory response,inhibit endometrial cell proliferation,lead to abnormal angiogenesis,and promote fibrosis.These changes disrupt endometrial structural integrity and physiological function,ulti-mately resulting in irreversible damage.This study clarifies the temporal dynamics of various indicators after injury and provides a ref-erence for identifying optimal intervention time points targeting inflammation and fibrosis,as well as strategies for promoting endome-trial repair.关键词
宫腔粘连/机械损伤/子宫内膜/纤维化/炎症反应Key words
intrauterine adhesion/mechanical injury/endometrium/fibrosis/inflammatory response引用本文复制引用
刘欣雨,王少为..机械损伤导致宫腔粘连的病理学研究[J].中国老年保健医学,2026,24(1):51-58,8.基金项目
中央高水平医院临床科研业务费资助项目(编号:BJ-2221-236) （编号:BJ-2221-236）
