姜黄素通过 TGF-β1/Smad3 通路抑制上皮-间质转化和成纤维细胞分化治疗子宫腺肌症

YANG Qing-mei; CHEN Yang; XIA Li-hua; XU Han; JIN Xiao-fen; WU Qing

doi:10.1007/s11655-025-4215-0

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姜黄素通过 TGF-β1/Smad3 通路抑制上皮-间质转化和成纤维细胞分化治疗子宫腺肌症

Original Article | Updated：2026-08-04

- 姜黄素通过 TGF-β1/Smad3 通路抑制上皮-间质转化和成纤维细胞分化治疗子宫腺肌症
- Curcumin Inhibits Fibroblast Differentiation and Epithelial-Mesenchymal Transition to Alleviate Adenomyosis through TGF-β1/Smad3 Pathway
- 中国结合医学杂志（英文版） 2026年32卷第5期页码：407-414
- Affiliations：
  
  1.Center for Reproductive Medicine, Department of Gynecology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou ( 310014), China
  2.Zhejiang Key Laboratory of Precision Diagnosis and Therapy for Major Gynecological Diseases, Women's Hospital, Zhejiang University School of Medicine, Hangzhou ( 310001), China
- Author bio：
  
  Prof. WU Qing, E-mail: okwq31@163.com
- Funds：
  
  Zhejiang Province Medical and Health Technology Plan Project(2021KY504;2023KY054;2025KY553);Zhejiang Key Laboratory of Precision Diagnosis and Therapy for Major Gynecological Diseases, Women's Hospital, Zhejiang University School of Medicine(ZDFY2022-CD-8)
- DOI：10.1007/s11655-025-4215-0
  中图分类号：
- 录用：2024-10-15，
  
  网络首发：2026-01-15，
  
  纸质出版：2026-05
- Accepted：
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YANG Qing-mei, CHEN Yang, XIA Li-hua, 等. 姜黄素通过 TGF-β1/Smad3 通路抑制上皮-间质转化和成纤维细胞分化治疗子宫腺肌症[J]. 中国结合医学杂志（英文版）, 2026,32(5):407-414.

YANG Qing-mei, CHEN Yang, XIA Li-hua, et al. Curcumin Inhibits Fibroblast Differentiation and Epithelial-Mesenchymal Transition to Alleviate Adenomyosis through TGF-β1/Smad3 Pathway[J]. Chinese Journal of Integrative Medicine, 2026, 32(5): 407-414.
YANG Qing-mei, CHEN Yang, XIA Li-hua, 等. 姜黄素通过 TGF-β1/Smad3 通路抑制上皮-间质转化和成纤维细胞分化治疗子宫腺肌症[J]. 中国结合医学杂志（英文版）, 2026,32(5):407-414. DOI： 10.1007/s11655-025-4215-0.

YANG Qing-mei, CHEN Yang, XIA Li-hua, et al. Curcumin Inhibits Fibroblast Differentiation and Epithelial-Mesenchymal Transition to Alleviate Adenomyosis through TGF-β1/Smad3 Pathway[J]. Chinese Journal of Integrative Medicine, 2026, 32(5): 407-414. DOI： 10.1007/s11655-025-4215-0.

摘要

目的：

探讨姜黄素（Cur）对子宫腺肌症（AM）的治疗作用及其机制。

方法：

新生ICR小鼠通过他莫昔芬（TAM）诱导子宫腺肌症模型。将24只新生雌性小鼠按随机数字表法随机分为对照组、模型组（TAM 1 mg/kg/天，第2-5天）、低剂量和高剂量姜黄素治疗组（TAM 1 mg/kg/天，第2-5天；姜黄素分别为50和200 mg/kg/天，第13-15周），每组6只。通过小鼠热板实验、子宫组织切片的苏木精-伊红（HE）染色、Masson 染色和 E-钙粘蛋白、N-钙粘蛋白、基质金属蛋白酶（MMP）9 和 MMP 11 的免疫组化染色来评估姜黄素的效果等。转化生长因子β1（TGF-β1）诱导 Ishikawa（IK）细胞发生表型改变，并在姜黄素处理后，通过实时荧光定量PCR和蛋白质印迹法检测E-钙粘蛋白、N-钙粘蛋白、MMP 9、MMP 11和p-Smad3/Smad3的mRNA和蛋白表达。

结果：

体内研究表明，姜黄素显著提高了小鼠痛阈（

0.01）。模型小鼠的子宫纤维化和异位腺体侵入程度显著高于对照组，高剂量姜黄素治疗后这些改变显著降低（

0.01）。高剂量姜黄素通过抑制子宫组织中TGF-β1的产生，逆转了E-钙粘蛋白的下降以及N-钙粘蛋白、MMP 9和MMP11水平的升高（

0.01）。体外研究中，姜黄素增强E-钙粘蛋白的蛋白表达，降低N-钙粘蛋白、MMP 9 和MMP11的蛋白表达（

0.01）。姜黄素有效抑制TGF-β1诱导的IK细胞Smad3的磷酸化（

0.01）。

结论：

姜黄素通过 TGF-β1/Smad3 通路抑制上皮-间质转化和成纤维细胞分化，进而治疗子宫腺肌症，这为非激素类药物治疗子宫腺肌症提供了一种新方法。

Abstract

Objective:

To investigate the therapeutic effects and mechanisms of curcumin (Cur) in adenomyosis (AM).

Methods:

A mouse uterine AM model was established by exposing ICR neonatal mice to tamoxifen (TAM). Female neonatal mice (day 1

=24) were numbered and randomly divided into control

model (TAM 1 mg/kg per day

day 2 to 5)

low- and high-doses Cur groups (TAM 1 mg/kg per day

day 2 to 5; Cur 50 and 200 mg/kg per day

respectively

week 13 to 15)

by a random number table

with 6 mice in each group. The effect of Cur was assessed by a hot-plate test on mice and uterine sections for hematoxylin and eosin (HE)

Masson staining

and immunohistochemistry staining of E-cadherin

N-cadherin

matrix metalloproteinases (MMP) 9 and MMP 11. Ishikawa (IK) cell phenotypic transformation was induced by transforming growth factor beta 1 (TGF-β1)

and the mRNA and protein expression

s of E-cadherin

N-cadherin

MMP 9

MMP 11 and p-Smad3/Smad3 were detected by quantitative real-time PCR and Western blot after Cur treatment.

Results:

In vivo

study results showed that Cur significantly improved pain tolerance (

0.01). The degrees of lesion fibrosis and invasion of ectopic glands in model mice were significantly higher than those in control mice

and the degrees were significantly reduced after high-dose Cur treatment (

0.01). High-dose Cur reversed the decrease of E-cadherin and the increase of the levels of N-cadherin

MMP 9 and MMP11 by inhibiting the production of TGF-β1 in the uterine tissue (

0.01).

In vitro

study

Cur increased the protein expression of E-cadherin and reduced the protein expressions of N-cadherin

MMP 9 and MMP 11 (

0.01). Cur effectively inhibited the phosphorylation of p-Smad3/Smad3 in IK cells induced by TGF-β1 (

0.01).

Conclusion:

Cur effectively alleviates AM and inhibits fibroblast differentiation and epithelial-mesenchymal transition by TGF-β1/Smad3 pathway

which provides a new approach for treating AM by non-hormonal drugs.

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