Estradiol valerate-induced endometrial hyperplasia is associated with oxidative stress and inflammatory activation
7 affiliations
- 1Department of Pharmacology, Faculty of Medicine, Minia University
- 2Department of pharmacology, faculty of medicine, Minia university
- 3Department of Pharmacology, Faculty of Medicine, Minia University, Minia, Egypt.
- 4Department of pharmacology, faculty of medicine, minia University, minia, Egypt.
- 5department of histology, faculty of medicine, Minia University, Minia, Egypt
- 6Pharmacology department, faculty of medicine, Minia university
- 7Pathology department, Faculty of Medicine, Minya University, Minya, Egypt
Abstract
Background: Endometrial hyperplasia (EH) is characterized by excessive proliferation of endometrial glands and may progress to endometrial carcinoma. While unopposed estrogen is the main etiological factor, oxidative stress and chronic inflammation are increasingly implicated in its pathogenesis and malignant transformation. Estradiol valerate (EV) is used experimentally to induce EH in rodents. Objective: To establish an EV-induced model of EH and to investigate associated changes in oxidative stress and inflammatory markers, providing a mechanistic basis for testing antioxidant and anti-inflammatory chemopreventive strategies. Methods: Ten adult female Wistar rats were randomized into control and EV-treated groups. EH was induced with EV 2 mg/kg/day orally for 10 days. Uterine weight and histopathology were assessed. Malondialdehyde (MDA) was measured as an oxidative stress marker and tumor necrosis factor-α (TNF-α) as an inflammatory marker in uterine tissue. Results: EV significantly increased uterine weight and induced histopathological features of EH compared to controls. This was accompanied by redox imbalance evidenced by elevated MDA and enhanced inflammatory signaling evidenced by elevated TNF-α. Conclusion: EV successfully induced EH with concomitant oxidative stress and inflammatory activation. The findings support the role of redox imbalance and inflammation in estrogen-induced endometrial proliferation and suggest that antioxidant and/or anti-inflammatory interventions warrant further investigation to limit EH progression and its carcinogenic potential.
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BibTeX
@article{abdelmonaem2026estradiol,
title = {{Estradiol valerate-induced endometrial hyperplasia is associated with oxidative stress and inflammatory activation}},
author = {Alyaa Abdelmonaem and Eman Kenawy and Maha Mickel and Hanaa Khalaf and Nada Mohammed and Asmaa Abdel- Aziz and Reham Mohammed},
journal = {Minia Journal of Medical Research},
year = {2026},
month = oct,
doi = {10.21608/mjmr.2026.536144.2402},
url = {https://doi.org/10.21608/mjmr.2026.536144.2402},
note = {CC BY},
}
RIS
TY - JOUR
TI - Estradiol valerate-induced endometrial hyperplasia is associated with oxidative stress and inflammatory activation
AU - Alyaa Abdelmonaem
AU - Eman Kenawy
AU - Maha Mickel
AU - Hanaa Khalaf
AU - Nada Mohammed
AU - Asmaa Abdel- Aziz
AU - Reham Mohammed
PY - 2026
DA - 2026/10/25
JO - Minia Journal of Medical Research
DO - 10.21608/mjmr.2026.536144.2402
UR - https://doi.org/10.21608/mjmr.2026.536144.2402
AB - Background: Endometrial hyperplasia (EH) is characterized by excessive proliferation of endometrial glands and may progress to endometrial carcinoma. While unopposed estrogen is the main etiological factor, oxidative stress and chronic inflammation are increasingly implicated in its pathogenesis and malignant transformation. Estradiol valerate (EV) is used experimentally to induce EH in rodents. Objective: To establish an EV-induced model of EH and to investigate associated changes in oxidative stress and inflammatory markers, providing a mechanistic basis for testing antioxidant and anti-inflammatory chemopreventive strategies. Methods: Ten adult female Wistar rats were randomized into control and EV-treated groups. EH was induced with EV 2 mg/kg/day orally for 10 days. Uterine weight and histopathology were assessed. Malondialdehyde (MDA) was measured as an oxidative stress marker and tumor necrosis factor-α (TNF-α) as an inflammatory marker in uterine tissue. Results: EV significantly increased uterine weight and induced histopathological features of EH compared to controls. This was accompanied by redox imbalance evidenced by elevated MDA and enhanced inflammatory signaling evidenced by elevated TNF-α. Conclusion: EV successfully induced EH with concomitant oxidative stress and inflammatory activation. The findings support the role of redox imbalance and inflammation in estrogen-induced endometrial proliferation and suggest that antioxidant and/or anti-inflammatory interventions warrant further investigation to limit EH progression and its carcinogenic potential.
SN - 2682-4558
ER -