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Polycystic Ovary Syndrome (PCOS) Animal Model

Polycystic Ovary Syndrome (PCOS) Animal Model

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Polycystic Ovary Syndrome
Reproductive system disease model

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Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Model Construction

Model Construction

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Polycystic Ovary Syndrome

Introduction to PCOS Animal Models

Animal models of polycystic ovary syndrome (PCOS) are predominantly established using rats and mice. Clinically, PCOS is a common gynecological disorder characterized by reproductive dysfunction, primarily driven by excessive ovarian androgen production. Following model induction, animals exhibit polycystic ovarian changes, hormonal imbalances, and ovulatory abnormalities, often accompanied by insulin resistance, obesity, and metabolic dysregulation—features that closely mirror the endocrine and reproductive‑metabolic characteristics of human PCOS. Consequently, these models are widely employed to investigate disease pathogenesis, screen therapeutic agents, and evaluate drug efficacy.

Advantages of Aniphe BioLab’s PCOS Animal Model Platform Services

Our platform boasts robust expertise in constructing animal models of polycystic ovary syndrome (PCOS) and stringent quality-control standards, fully meeting the needs of both research studies and new‑drug development.

Comprehensive model coverage

Typical model phenotype

Following model induction, the animals exhibit prominent features such as sex hormone dysregulation, polycystic ovarian changes, and ovulatory dysfunction, with stable and highly reproducible experimental parameters.

Standardization of the modeling process

Standardized Feeding and Management

Throughout the entire study, animals were maintained under standardized husbandry conditions, with regular monitoring of body weight, estrous cycles, and hormone levels; experimental data are fully traceable.

Multidimensional Evaluation System

Comprehensive multi-dimensional detection capabilities

It supports a range of diagnostic assessments, including sex hormone biochemistry, ovarian histopathology, carbohydrate and lipid metabolism, and molecular biology.

Adapted for multi-cycle studies

The solution is flexible and customizable.

The dosage, modeling cycle, and intervention duration can be flexibly adjusted to accommodate various experimental designs.

One-stop closed-loop service

We independently handle the entire workflow, from model generation and routine monitoring to sample analysis, thereby supporting both basic research and preclinical development programs.

Modeling cycle

4–6 weeks

1  Laboratory animals

SPF-grade rats

1  Positive drug

Metformin

1  Application areas

It is widely applied in studies of disease pathogenesis, investigations into the mechanisms of hyperandrogenism and insulin resistance, research on follicular development abnormalities and ovulation disorders, the regulation of reproductive endocrinology, disorders of carbohydrate and lipid metabolism and obesity-related research, as well as in the evaluation of pharmacological efficacy and the elucidation of mechanisms of action for traditional Chinese medicines, natural products, small-molecule compounds, biologics, and innovative drugs.

Construction of a PCOS Animal Model

Animal models of polycystic ovary syndrome (PCOS) are primarily established by inducing hyperandrogenism and/or hyperestrogenism. Hyperandrogenic models typically involve chronic administration of agents such as letrozole, dehydroepiandrosterone (DHEA), or testosterone propionate, which elicit hallmark PCOS phenotypes—including hyperandrogenemia, disrupted estrous cycles, polycystic ovarian changes, and insulin resistance—thus closely mimicking the clinical features of the disease. Hyperestrogenic models, on the other hand, often employ either continuous or single-dose administration of estradiol valerate to suppress normal ovulation and follicular development, thereby generating a polycystic‑like ovarian phenotype; these models are mainly used to investigate PCOS‑associated ovarian dysfunction and reproductive endocrine alterations.

Model features:

The phenotypes observed in the two modeling approaches share similarities with human polycystic ovary syndrome, yet they still exhibit certain limitations; it is important to consider the distinct pathogenic features of each model.

Metformin Treatment Data

Overall, the PCOS‑model mice exhibited a range of hallmark pathological features, including obesity, impaired glucose tolerance, and insulin resistance. Treatment with the classic positive control drug metformin reduced body weight, improved abnormal glucose metabolism, and reversed insulin resistance, thereby validating metformin’s therapeutic efficacy in addressing the metabolic disturbances associated with PCOS.

 

 

This study used seven consecutive days of vaginal smears to assess the estrous cycle in mice. Figure D illustrates the vaginal cytological features corresponding to the four phases—proestrus, estrus, metestrus, and diestrus. In the control group, estrous staging fluctuated regularly with day‑to‑day variation, indicating a normal cyclical progression; by contrast, the PCOS model group exhibited prolonged arrest of estrous stages, disrupted cycling, and ovulatory dysfunction. Following treatment with metformin, estrous staging resumed its periodic oscillations, and the estrous rhythm was restored. These findings demonstrate that PCOS modeling can induce arrest of the estrous cycle in mice, while metformin can rectify the dysregulated cycle and ameliorate reproductive abnormalities associated with ovulatory dysfunction in the animal model.

 

 

PCOS modeling induces abnormal follicular development in the mouse ovary, leading to polycystic‑like pathological changes and dysregulation of sex hormone secretion; metformin can ameliorate the polycystic ovarian morphology, optimize folliculogenesis, and modulate reproductive endocrine parameters, thereby alleviating both the ovarian pathology and endocrine disturbances associated with PCOS.

 

 

PCOS modeling suppresses the transcription and protein expression of GPX4 and SIRT3 in ovarian tissue; metformin upregulates the mRNA and protein levels of these two molecules. It is hypothesized that the upregulation of GPX4 and SIRT3, along with the amelioration of ferroptosis‑related processes, constitutes a key molecular mechanism by which metformin alleviates ovarian damage in PCOS.

 

 

The pathological state of PCOS suppresses AMPK phosphorylation, disrupts mTOR signaling, and leads to aberrant hyperactivation of autophagy. Metformin can activate AMPK, modulate the downstream mTOR pathway, and downregulate Beclin‑1, thereby restoring dysregulated autophagic homeostasis—this represents one of the key molecular mechanisms by which metformin ameliorates ovarian pathology in PCOS.

 

 

References: Metformin improves polycystic ovary syndrome in mice by inhibiting ovarian ferroptosis.