Association of ovarian inflammation and hormonal dysregulation: a candidate mechanism underlying polycystic ovary syndrome.
7 affiliations
- 1College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, 010018, P.R. China.
- 2Key Laboratory of Animal Embryo and Development Engineering of Autonomous Region Universities, Inner Mongolia Agricultural University, Hohhot, 010018, P.R. China.
- 3Inner Mongolia Key Laboratory of Veterinary Fundamentals and Disease Control of Herbivorous livestock, Hohhot, 010018, P.R. China.
- 4Department of Neurology, The Second Affiliated Hospital of Inner, Mongolia Medical University, Hohhot, 010030, P.R. China.
- 5College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, 010018, P.R. China. [email protected].
- 6Key Laboratory of Animal Embryo and Development Engineering of Autonomous Region Universities, Inner Mongolia Agricultural University, Hohhot, 010018, P.R. China. [email protected].
- 7Inner Mongolia Key Laboratory of Veterinary Fundamentals and Disease Control of Herbivorous livestock, Hohhot, 010018, P.R. China. [email protected].
Abstract
Background
Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by female infertility, menstrual irregularities, and hormonal imbalance, leading to impaired reproductive health. Hyperandrogenemia is considered a central endocrine feature and a key contributor to PCOS pathophysiology.Results
A dehydroepiandrosterone (DHEA)-induced mouse model was established to investigate transcriptomic alterations in granulosa cells (GCs) and their association with endocrine and inflammatory changes in PCOS. Model validation was performed using histological analysis (H&E staining), estrous cycle analysis, Western blotting of estrogen receptors (ERα and ERβ), and serum hormone profiling by ELISA. The PCOS model exhibited typical phenotypes, including polycystic ovarian morphology, estrous cycle arrest, and elevated testosterone (T), luteinizing hormone (LH), and LH/FSH ratios. Increased ERα expression was observed in ovarian GCs. RNA sequencing (RNA-seq) identified 161 differentially expressed genes, enriched in TNF signaling, NF-κB signaling, and steroid hormone biosynthesis pathways. In vitro, T-treated primary GCs showed increased ERα/ERβ ratio and enhanced pro-inflammatory signaling, with suppression of anti-inflammatory markers, consistent with in vivo findings. Overall, these findings support an association between endocrine alterations and inflammatory responses in ovarian GCs during PCOS.Conclusions
In conclusion, inflammatory factor expression in GCs was significantly associated with reproductive hormone dysregulation in PCOS, suggesting a potential hormone-inflammation interaction axis in the pathophysiology of PCOS.
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BibTeX
@article{hao2026association,
title = {{Association of ovarian inflammation and hormonal dysregulation: a candidate mechanism underlying polycystic ovary syndrome.}},
author = {Shaoyu Hao and Jing Pan and Qi Zhao and Yisi A and Haijun Li},
journal = {Journal of ovarian research},
year = {2026},
month = aug,
doi = {10.1186/s13048-026-02218-3},
url = {https://europepmc.org/article/MED/42958542},
note = {CC BY},
}
RIS
TY - JOUR
TI - Association of ovarian inflammation and hormonal dysregulation: a candidate mechanism underlying polycystic ovary syndrome.
AU - Shaoyu Hao
AU - Jing Pan
AU - Qi Zhao
AU - Yisi A
AU - Haijun Li
PY - 2026
DA - 2026/08/04
JO - Journal of ovarian research
DO - 10.1186/s13048-026-02218-3
UR - https://europepmc.org/article/MED/42958542
AB - Background Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by female infertility, menstrual irregularities, and hormonal imbalance, leading to impaired reproductive health. Hyperandrogenemia is considered a central endocrine feature and a key contributor to PCOS pathophysiology.Results A dehydroepiandrosterone (DHEA)-induced mouse model was established to investigate transcriptomic alterations in granulosa cells (GCs) and their association with endocrine and inflammatory changes in PCOS. Model validation was performed using histological analysis (H&E staining), estrous cycle analysis, Western blotting of estrogen receptors (ERα and ERβ), and serum hormone profiling by ELISA. The PCOS model exhibited typical phenotypes, including polycystic ovarian morphology, estrous cycle arrest, and elevated testosterone (T), luteinizing hormone (LH), and LH/FSH ratios. Increased ERα expression was observed in ovarian GCs. RNA sequencing (RNA-seq) identified 161 differentially expressed genes, enriched in TNF signaling, NF-κB signaling, and steroid hormone biosynthesis pathways. In vitro, T-treated primary GCs showed increased ERα/ERβ ratio and enhanced pro-inflammatory signaling, with suppression of anti-inflammatory markers, consistent with in vivo findings. Overall, these findings support an association between endocrine alterations and inflammatory responses in ovarian GCs during PCOS.Conclusions In conclusion, inflammatory factor expression in GCs was significantly associated with reproductive hormone dysregulation in PCOS, suggesting a potential hormone-inflammation interaction axis in the pathophysiology of PCOS.
SN - 1757-2215
ER -