CXCL12 promotes endometrial repair through MSC homing in a mouse model of  intrauterine adhesions: Multimechanistic study based on angiogenesis, cell proliferation and Sirt1 upregulation

SHAO Kangning; WANG Yaqin; ZHAO Dongmei; SONG Yuxia

doi:10.16016/j.2097-0927.202511072

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CXCL12 promotes endometrial repair through MSC homing in a mouse model of intrauterine adhesions: Multimechanistic study based on angiogenesis, cell proliferation and Sirt1 upregulation

Basic Medicine | 更新时间：2026-02-23

- CXCL12 promotes endometrial repair through MSC homing in a mouse model of intrauterine adhesions: Multimechanistic study based on angiogenesis, cell proliferation and Sirt1 upregulation
- Journal of Army Medical University Vol. 48, Issue 3, Pages: 305-316(2026)
- 作者机构：
  
  郑州大学第二附属医院生殖医学部，河南郑州
- 作者简介：
  
  WANG Yaqin， E-mail： 576341948@qq.com
- 基金信息：
  
  the Project of Science and Technology Research of Henan Province(242102310364)
- DOI：10.16016/j.2097-0927.202511072
  CLC： R322.65;R394.2;R711.74
- Received：13 November 2025，
  
  Revised：2026-01-07，
  
  Accepted：14 January 2026，
  
  Published：15 February 2026
- 稿件说明：
移动端阅览
邵康宁，王亚芹，赵冬梅，等.趋化因子CXCL12通过促进间充质干细胞归巢修复宫腔粘连小鼠子宫内膜：基于血管生成、细胞增殖及Sirt1上调的多机制研究［J］.陆军军医大学学报，2026，48（03）：305-316.DOI：10.16016/j.2097-0927.202511072.

SHAO K N， WANG Y Q， ZHAO D M，et al.CXCL12 promotes endometrial repair through MSC homing in a mouse model of intrauterine adhesions： Multimechanistic study based on angiogenesis， cell proliferation and Sirt1 upregulation［J］.J Army Med Univ，2026，48（03）：305-316.DOI：10.16016/j.2097-0927.202511072.
邵康宁，王亚芹，赵冬梅，等.趋化因子CXCL12通过促进间充质干细胞归巢修复宫腔粘连小鼠子宫内膜：基于血管生成、细胞增殖及Sirt1上调的多机制研究［J］.陆军军医大学学报，2026，48（03）：305-316.DOI：10.16016/j.2097-0927.202511072. DOI：

SHAO K N， WANG Y Q， ZHAO D M，et al.CXCL12 promotes endometrial repair through MSC homing in a mouse model of intrauterine adhesions： Multimechanistic study based on angiogenesis， cell proliferation and Sirt1 upregulation［J］.J Army Med Univ，2026，48（03）：305-316.DOI：10.16016/j.2097-0927.202511072. DOI：

摘要

目的

探索CXCL12在促进宫腔粘连（intrauterine adhesions， IUA）术后子宫内膜修复中的作用。

方法

采用机械刮宫法构建IUA小鼠模型。将48只7~8周龄C57BL/6健康雌性小鼠（体质量18~20 g）采用区组随机法分为4组（

=12）：假手术组（Sham组）、模型组（Model组）、脐带间充质干细胞（umbilical cord-derived mesenchymal stem cells，UC-MSCs）治疗组及CXCL12治疗组。Sham组仅切开腹壁，不进行宫腔操作；Model组机械刮宫后向宫腔内灌注100 μL生理盐水溶液；UC-MSCs治疗组机械刮宫后宫腔灌注UC-MSCs悬液100 μL（含1×10

个细胞）；CXCL12治疗组机械刮宫后灌注CXCL12溶液100 μL（含200 ng CXCL12）。造模后7 d，通过组织学验证造模成果；通过免疫荧光染色评估CXCL12对MSCs的趋化作用。造模后21 d，通过HE染色计算子宫内膜厚度、腺体数目；Masson染色评估子宫内膜纤维化面积；免疫组织化学染色测定微血管密度（microvessel density，MVD）、血管内皮生长因子（vascular endothelial growth factor， VEGF）、Ki-67、沉默信息调节因子1（sirtuin 1， Sirt1）的表达水平；采用Spearman相关系数验证Sirt1表达水平和子宫内膜纤维化的相关性。

结果

造模后7 d，经组织学验证IUA小鼠模型造模成功；各组免疫荧光结果显示：CXCL12治疗组和UC-MSCs治疗组小鼠子宫内膜归巢的MSCs数量比Sham组和Model组显著增加（

0.001），两治疗组组间MSCs数量比较无显著差异。造模后21 d，各组子宫内膜厚度及腺体数量比较显示：CXCL12治疗组和UC-MSCs治疗组的子宫内膜厚度（

0.001）及腺体数量（

0.05）较Model组显著增加。小鼠子宫内膜纤维化程度比较结果显示：CXCL12治疗组和UC-MSCs治疗组的子宫内膜纤维化程度较Model组均明显降低（

0.001）。造模后21 d，MVD结果显示：CXCL12治疗组及UC-MSCs治疗组的MVD均显著高于Model组（

0.05）。免疫组化VEGF平均光密度值分析显示：UC-MSCs治疗组和CXCL12治疗组的VEGF表达均显著高于Model组（

0.001）。Ki-67平均光密度值分析显示：与Model组相比，Ki-67表达水平在UC-MSCs治疗组和CXCL12治疗组均显著升高（

0.001）。Sirt1平均光密度值分析显示：CXCL12治疗组和UC-MSC治疗组的Sirt1表达较Model组均显著升高（

0.001）；控制分组变量后，Sirt1表达水平和子宫内膜纤维化面积存在显著负相关（

=-0.73，

0.05，

=-3.86）。

结论

CXCL12通过促进MSC归巢至IUA小鼠子宫内膜，发挥与UC-MSCs疗法相似的作用，能够有效促进子宫内膜修复并减少间质纤维化，且Sirt1表达上调可能参与此过程。

Abstract

Objective

To investigate CXCL12 therapeutic potential in endometrial repair post intrauterine adhesion (IUA) surgery.

Methods

A murine model of IUA was established using mechanical curettage. A total of 48 healthy female C57BL/6 mice (aged 7 to 8 weeks

weighing 18 to 20 g) were randomly allocated to 4 groups (

=12 per group): the sham-operated group (Sham)

the model group (Model)

the umbilical cord mesenchymal stem cell treatment group (UC-MSCs treatment group)

and the CXCL12 treatment group. In the Sham group

only the abdominal wall was incised without intrauterine manipulation. In the Model group

after mechanical curettage

100 μL of normal saline was infused into the uterine cavity. In the UC-MSCs treatment group

after curettage

100 μL of UC-MSCs suspension (1×10⁶ cells) was infused into the uterine cavity. In the CXCL12 treatment group

after curettage

100 μL of CXCL12 solution (containing 200 ng CXCL12) was infused into the uterine cavity. At 7 d post-modeling

histological examination was performed to confirm model establishment

and immunofluorescence staining was used to assess the chemotactic effect of CXCL12 on MSCs. At 21 d post-modeling

hematoxylin and eosin (HE) staining was used to evaluate endometrial thickness and gland number; Masson’s trichrome staining assessed the extent of endometrial fibrosis. Immunohistochemical staining was employed to determine the microvessel density (MVD) and the expression levels of VEGF

Ki-67

and Sirt1. Spearman correlation coefficient was used to assess the correlation between Sirt1 expression levels and endometrial fibrosis.

Results

At 7 d post-modeling

histological examination confirmed the successful establishment of the IUA mouse model. Immu

nofluorescence staining demonstrated significantly increased MSC homing to the endometrium in both the CXCL12 and UC-MSCs treatment groups versus the Sham and Model groups (

0.001)

with no significant difference between the 2 treatment groups. At 21 d post-modeling

both the CXCL12 and UC-MSCs treatment groups exhibited significantly greater endometrial thickness (

0.001) and gland number (

0.05) relative to the Model group. Endometrial fibrosis was significantly reduced in the treatment groups compared with the Model group (

0.001). Microvessel density (MVD) was significantly higher in the CXCL12 and UC-MSCs groups than in the Model group (

0.05). Immunohistochemical analysis revealed significantly elevated expression of VEGF (

0.001)

Ki-67 (

0.001)

and Sirt1 (

0.001) in both treatment groups versus the Model group. After controlling for group allocation

Sirt1 expression showed a significant negative correlation with endometrial fibrosis area (

=-0.73

0.05

=-3.86).

Conclusions

Through enhancing MSC homing to the endometrium in IUA mice

CXCL12 exerts therapeutic effects comparable to UC-MSCs therapy

effectively promoting endometrial regeneration and reducing stromal fibrosis

with upregulated Sirt1 expression potentially mediating these effects.

关键词

Keywords

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