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

Abstract

Objective

This study aimed 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. After three weeks, mice were euthanized, and histopathological examination was performed using hematoxylin and eosin (HE) staining. , and the expression level of S-adenosylmethionine (SAM) was measured using enzyme-linked immunosorbent assay (ELISA). Immunohistochemistry was employed to evaluate the expressions of Ki67, vimentin, vascular endothelial growth factor (VEGF), and Caspase-1.

Results

The endometriosis mice model was successfully established and characterized by ectopic lesions displaying transparent or red vesicular or nodular features with a visible vascular network on the surface. In the model group, endometrial epithelial hyperplasia exhibited columnar morphology, increased mesenchymal cell numbers, and regular cell morphology. Conversely, in the medication group, endometrial stromal cell numbers were sparse, cell morphology was irregular, and numerous vacuoles were observed in the endometrial tissue, indicative of apoptotic cell morphology changes. . MAT2A, PRMT5, cyclin D1, and C-MYC expressions were increased, and vimentin, Ki67, VEGF, and caspase-1 expressions were strongly positive, with statistically significant differences (P < 0.05). In contrast, compared to the model group, the quercetin intervention group exhibited significantly reduced ectopic lesion weights, increased PPARγ expression, and significantly reduced protein expression levels of MAT2A, PRMT5, SAM, cyclin D1, and C-MYC. Furthermore, expressions of vimentin, Ki67, VEGF, and caspase-1 were weakly positive, with statistically significant differences (P < 0.05).

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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2025-02-24
2025-04-24

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Quercetin Inhibits Ectopic Lesion Formation in Mice by Modulating the MAT2A/PRMT5 Pathway through PPARγ Activation
Bentham Science Publishers ; https://doi.org/10.2174/0113862073379671250219103011
/content/journals/cchts/10.2174/0113862073379671250219103011
/content/journals/cchts/10.2174/0113862073379671250219103011
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  • Article Type:     Research Article
Keywords: MAT2A ; PRMT5 ; PPARγ ; Endometriosis ; quercetin

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