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Updated: Aug 5, 2026
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A Modified Technique for Inducing Polycystic Ovary Syndrome in Mice
Published on: July 5, 2024
Scutellarin ameliorates PCOS in a mouse model by restoring mitochondrial function and inhibiting granulosa cell
Zhi Li1,2, Xiaoping Yang3, Weifen Deng4
1Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Ganzhou Hospital, Guangdong Academy of Medical Sciences , Guangzhou, China.
The Journal of Endocrinology
|August 3, 2026
Summary
Scutellarin improves metabolic and reproductive issues in polycystic ovary syndrome (PCOS) by reducing granulosa cell apoptosis and enhancing mitochondrial function. This flavonoid shows promise for treating PCOS-related ovarian and systemic dysfunctions.
Area of Science:
- Endocrinology
- Reproductive Biology
- Mitochondrial Biology
Background:
- Polycystic ovary syndrome (PCOS) is a prevalent endocrine-metabolic disorder with limited therapeutic options.
- Granulosa cell (GC) apoptosis and mitochondrial dysfunction are key contributors to ovarian dysfunction in PCOS.
- Scutellarin, a flavonoid, is a potential but uninvestigated therapeutic agent for PCOS.
Purpose of the Study:
- To investigate the therapeutic potential of scutellarin in a dehydroepiandrosterone (DHEA)-induced PCOS mouse model and in vitro.
- To elucidate the molecular mechanisms underlying scutellarin's effects on PCOS-related abnormalities.
- To assess scutellarin's impact on metabolic parameters, reproductive function, ovarian histology, and fertility.
Main Methods:
- Utilized a DHEA-induced PCOS mouse model and DHEA-treated human granulosa-like KGN cells.
- Assessed metabolic and reproductive parameters, ovarian histology, and fertility.
- Employed transcriptomics, qRT-PCR, Western blotting, TUNEL staining, flow cytometry, and mitochondrial assays to evaluate molecular mechanisms, apoptosis, and mitochondrial function.
Main Results:
- Scutellarin treatment improved metabolic phenotypes (glucose intolerance, insulin resistance), normalized estrous cycles, reduced testosterone and LH levels, enhanced ovarian morphology, and improved fertility in PCOS mice.
- Mechanistically, scutellarin reduced GC apoptosis (BCL2, BAX, cleaved Caspase-3) and modulated the PI3K/Akt signaling pathway.
- In vitro, scutellarin improved mitochondrial function in DHEA-treated KGN cells by reducing ROS production and restoring membrane potential.
Conclusions:
- Scutellarin ameliorates metabolic and reproductive abnormalities in a PCOS mouse model.
- The therapeutic effects are linked to reduced GC apoptosis and improved mitochondrial function.
- Scutellarin demonstrates potential for dual benefits on ovarian and systemic dysfunctions in PCOS, warranting clinical investigation.
