Quercetin Inhibits Ectopic Lesion Formation in Mice by Modulating the MAT2A/PRMT5 Pathway through PPARγ Activation

Shun Zhang, Yuan-Yuan Zhang, Qiu-Xia Zeng, Li Wang, Kong-Xian Li, Qi Chen
Combinatorial chemistry & high throughput screening · 2026 · vol. 29(1) , pp. 150–160 · doi:10.2174/0113862073379671250219103011 · PMID:39995138
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⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

Quercetin treatment in mice reduced endometriosis lesion formation by activating PPARγ, which modulated the MAT2A/PRMT5 pathway and promoted apoptosis of ectopic endometrial cells.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 · read from full text ⓘ

The paper studied the effects of quercetin in a C57BL/6 mouse endometriosis model, comparing sham, untreated model, and daily quercetin gavage (100 mg/kg/d) groups, with lesion histopathology (HE), ultrastructure (electron microscopy), and protein expression assessed by Western blotting and immunohistochemistry. Quercetin treatment was associated with reduced ectopic lesion weight and histological changes consistent with apoptosis, including decreased PPARγ- and MAT2A/PRMT5-pathway–related proteins (MAT2A, PRMT5, cyclin D1, C-MYC) and changes in apoptosis/cell-viability markers (caspase-1, Ki67, VEGF, vimentin), while PPARγ increased. A stated limitation is that SAM expression was reported as unchanged between sham and model despite pathway discussion, indicating that not all related measures shifted. This paper is centrally about endometriosis — it tests quercetin’s ability to reduce ectopic lesion formation by modulating the MAT2A/PRMT5 pathway via PPARγ activation.

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Abstract

INTRODUCTION: This study aimed to examine the impact of quercetin on a mouse model of endometriosis and elucidate its underlying mechanisms. METHODS: An endometriosis model was established using C57BL/6 mice, which were divided into three groups: 1) sham group, 2) model group, and 3) model group treated with daily gavage administration of 100 mg/kg/d quercetin. Histopathological examination was performed using hematoxylin and eosin (HE) staining. The microstructure of the lesions was examined using electron microscopy. The expressions levels of related proteins, such as the peroxisome proliferator- activated receptor-γ (PPARγ), methionine adenosyl-transferase 2A (MAT2A), Ki67 and VEGF was measured using Western blotting or Immunohistochemistry. RESULTS: Compared to the model group, the medication group showed sparse endometrial stromal cells, irregular morphology, and numerous vacuoles, indicating apoptosis. Compared to the sham group, SAM expression was unchanged (P > 0.05), while PPARγ decreased. MAT2A, PRMT5, cyclin D1, and C-MYC increased, and vimentin, Ki67, VEGF, and caspase-1 were strongly positive (P < 0.05). Quercetin intervention reduced ectopic lesion weights, increased PPARγ, and decreased MAT2A, PRMT5, SAM, cyclin D1, and C-MYC. Vimentin, Ki67, VEGF, and caspase-1 were weakly positive (P < 0.05). DISCUSSION: These results indicate that quercetin effectively reduced endometriosis lesions by modulating key protein expressions and promoting apoptosis. CONCLUSION: Quercetin modulated the transcription of the MAT2A/PRMT5 gene by activating PPARγ activity, thereby influencing the ectopic implantation and growth of endometrial cells.
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Abstract

Introduction: This study aimed to examine the impact of quercetin on a mouse model of endometriosis and elucidate its underlying mechanisms.

Methods

An endometriosis model was established using C57BL/6 mice, which were divided into three groups: 1) sham group, 2) model group, and 3) model group treated with daily gavage administration of 100 mg/kg/d quercetin. Histopathological examination was performed using hematoxylin and eosin (HE) staining. The microstructure of the lesions was examined using electron microscopy. The expressions levels of related proteins, such as the peroxisome proliferator- activated receptor-γ (PPARγ), methionine adenosyl-transferase 2A (MAT2A), Ki67 and VEGF was measured using Western blotting or Immunohistochemistry.

Results

Compared to the model group, the medication group showed sparse endometrial stromal cells, irregular morphology, and numerous vacuoles, indicating apoptosis. Compared to the sham group, SAM expression was unchanged (P > 0.05), while PPARγ decreased. MAT2A, PRMT5, cyclin D1, and C-MYC increased, and vimentin, Ki67, VEGF, and caspase-1 were strongly positive (P < 0.05). Quercetin intervention reduced ectopic lesion weights, increased PPARγ, and decreased MAT2A, PRMT5, SAM, cyclin D1, and C-MYC. Vimentin, Ki67, VEGF, and caspase-1 were weakly positive (P < 0.05).

Discussion

These results indicate that quercetin effectively reduced endometriosis lesions by modulating key protein expressions and promoting apoptosis.

Conclusion

Quercetin modulated the transcription of the MAT2A/PRMT5 gene by activating PPARγ activity, thereby influencing the ectopic implantation and growth of endometrial cells.

Keywords

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Methionine Adenosyltransferase Methionine Adenosyltransferase Methionine Adenosyltransferase Methionine Adenosyltransferase Methionine Adenosyltransferase Methionine Adenosyltransferase Methionine Adenosyltransferase Methionine Adenosyltransferase

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