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Quercetin Inhibits Ectopic Lesion Formation in Mice by Modulating the MAT2A/PRMT5 Pathway through PPARγ Activation
Shun Zhang1, Yuan-Yuan Zhang2, Qiu-Xia Zeng2
1Departments of General Surgery, The First Affiliated Hospital of Nanchang University, Nanchang 330000, Jiangxi Province, China.
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.
Insights
Quercetin treatment reduced endometriosis lesion weight and proliferation in mice by activating PPARγ, decreasing MAT2A/PRMT5 gene transcription, and inhibiting endometrial cell growth.
Area of Science:
- Reproductive biology
- Molecular mechanisms of disease
- Natural product pharmacology
Background:
- Endometriosis is a debilitating gynecological condition characterized by ectopic endometrial tissue.
- Current treatments for endometriosis have limitations, necessitating the exploration of novel therapeutic agents.
- Quercetin, a plant flavonoid, has demonstrated anti-inflammatory and anti-proliferative properties.
Purpose of the Study:
- To investigate the therapeutic effects of quercetin on a mouse model of endometriosis.
- To elucidate the molecular mechanisms underlying quercetin's action in endometriosis.
Main Methods:
- Establishment of a murine endometriosis model.
- Administration of quercetin (100 mg/kg/d) via gavage for three weeks.
- Histopathological analysis (HE staining), electron microscopy, ELISA, Western blotting, and immunohistochemistry were performed.
Main Results:
- Quercetin significantly reduced ectopic lesion weight and suppressed endometrial cell proliferation.
- Quercetin increased peroxisome proliferator-activated receptor-γ (PPARγ) expression.
- Quercetin decreased the expression of methionine adenosyl-transferase 2A (MAT2A), protein arginine methyltransferase 5 (PRMT5), and related proteins involved in cell growth and angiogenesis.
Conclusions:
- Quercetin exerts therapeutic effects on endometriosis by modulating the MAT2A/PRMT5 pathway through PPARγ activation.
- Quercetin shows potential as a novel therapeutic agent for endometriosis.
