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Mentha spicata and Its Bioactive Compound Carvone Ameliorate Metabolic Disturbance and Ovarian Dysfunction in
Comfort A Oladele1, Stephanie E Areloegbe1, Chidubem F Emereonye1
1Afe Babalola University, Ado-Ekiti, Nigeria.
Problem:
Polycystic ovarian syndrome (PCOS) is a common endocrine and metabolic disorder in women of child-bearing age, often linked to ovarian dysfunction and complications beyond infertility. However, its management remains suboptimal due to unclear etiology. Sterol Regulatory Element Binding Protein 1 (SREBP1) and Toll-like Receptor 4 (TLR4) have been implicated in lipid metabolism and immune responses, but their interaction with ovarian function in PCOS remains unclear. Mentha spicata (spearmint) traditionally recognized for its hormonal and metabolic benefits, and its bioactive component, carvone (CARV), exhibit potent antioxidant and anti-inflammatory properties.
Method Of Study:
This study investigated the involvement of SREBP1/TLR4-dependent pathway in letrozole-induced PCOS rat model and assessed the therapeutic potential of Mentha spicata extract (MENT) and carvone. Eight-week-old female Wistar rats were divided into groups (n = 7), namely, Control, CARV, MENT, PCOS, PCOS+CARV, and PCOS+MENT groups. Administration of letrozole (1 mg/kg) for 3 weeks induced PCOS. Thereafter, rats were treated with MENT (100 mg/kg, po) and carvone (20 mg/kg, po) for 6 weeks.
Result:
The PCOS rats exhibited elevated plasma testosterone, anti-Mullerian hormone, prolactin, sex hormone-binding globulin, luteinizing hormone, lipid profiles, insulin resistance (HOMA-IR), and ovarian inflammation (NF-κB)/lipid peroxidation (malondialdehyde), alongside reduced antioxidant levels (glutathione) and increased Galectin-3 expression. Furthermore, there was an upregulation of SREBP1 and TLR4. Treatment with MENT or carvone significantly reversed these systemic and ovarian abnormalities compared to PCOS group.
Conclusion:
These findings suggest that M. spicata and carvone ameliorate metabolic disturbance and ovarian dysfunction in PCOS by suppressing SREBP1/TLR4 expression.
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