Curcumin Mitigates Polycystic Ovary Syndrome in Mice by Suppressing TLR4/MyD88/NF-κB Signaling Pathway Activation and Reducing Intestinal Mucosal Permeability

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Abstract

Polycystic ovary syndrome (PCOS) stands as a prevalent endocrine-metabolic disorder impairing female fertility, often intertwined with alterations in intestinal mucosal barrier integrity and chronic inflammation. Curcumin, renowned for its multifaceted biological activities including anti-inflammatory, anti-tumor, and antioxidant properties, emerges as a potential therapeutic agent for PCOS. In this study, we investigated the effects and underlying mechanisms of curcumin in mitigating PCOS in mice. The PCOS mouse model was induced by administering dehydroepiandrosterone (DHEA) dissolved in soybean oil (6mg/100g BW) for 20 days, followed by a 45-day intervention period with curcumin. Subsequent euthanasia enabled examination of relevant indicators. Evaluation encompassed ovarian and colonic morphology, intestinal mucosal barrier function, and the TLR4/MyD88/NF-κB signaling pathway in each experimental group. Our findings indicate that curcumin holds promise in alleviating PCOS symptoms. By inhibiting the activation of the TLR4/MyD88/NF-κB signaling pathway and reducing intestinal mucosal permeability, curcumin demonstrates potential as a clinical intervention for this disorder. These findings highlight the therapeutic potential of curcumin in managing PCOS and warrant further clinical investigation to validate its efficacy.

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