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Updated: Sep 21, 2026
Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue
Published on: January 6, 2012
The effects of isoliquiritigenin on endometriosis in vivo and in vitro study
Yi-Wen Hsu1, Hsin-Yuan Chen1, Yi-Fen Chiang1
1School of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 11031, Taiwan.
Background:
Endometriosis is a common gynaecological disease characterized by growth of uterine endometrial tissue, outside the uterine cavity, on the ovaries, oviduct and pelvic peritoneum. Isoliquiritigenin (ISL) is a natural flavonoid isolated from the root of licorice (Glycyrrhiza uralensis) and shallot (Allium cepa). ISL has previously shown antioxidant, anti-inflammatory, anti-proliferation and anti-tumor activities.
Purpose:
This study aimed to investigate the effects of ISL on endometriosis in vivo and in vitro.
Methods:
End1/E6E7 endometriosis cells were treated with ISL and β-estradiol. The MTT assay was used to detect cell viability. Cell migration was evaluated by the wound-healing assay. The expression of epithelial-to-mesenchymal transition (EMT)-related proteins were detected by western blot. Female Balb/c mice, surgically induced to have endometriosis by transplanting uterine tissue into the abdominal cavity, were treated with ISL or vehicle for 4 weeks. Lesion growth was subsequently analyzed by high-resolution ultrasound imaging. Serum and lesion inflammatory cytokines were measured by ELISA. EMT-related proteins and apoptosis-related proteins of endometriotic lesions were detected by western blot.
Results:
It was observed that ISL treatment inhibited the viability and migration of End1/E6E7. ISL treatment increased the expression of E-cadherin, and decreased the expression of N-cadherin, Slug and Snail. In the animal model, ISL treatment reduced the volume and weight of endometriotic lesions, decreased serum and lesion inflammatory cytokines, inhibited EMT, and induced apoptosis of the lesions.
Conclusion:
ISL inhibited the viability, migration and EMT-related proteins of End1/E6E7 cells, reduced the volume and weight of endometriotic lesions, inhibited inflammatory cytokines and EMT, and induced apoptosis of the lesions to improve endometriosis.
