ArticleFrontiers in immunology2026
Gui Shen Wan ameliorates PCOS-like cellular phenotypes by suppressing TNF-α-mediated inflammation and restoring the PI3K/Akt signaling pathway.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- FAAH as a Molecular Regulator of Endocannabinoid Signaling: Mechanistic Insights into Reproductive, Metabolic, and Inflammatory Dysfunctions in Polycystic Ovary Syndrome.Molecules (Basel, Switzerland) · 2026Review
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Authors and funding
6 authors.
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Abstract
Background: Polycystic ovary syndrome (PCOS) is associated with chronic low-grade inflammation and insulin signaling dysregulation. Gui Shen Wan (GSW), a traditional Chinese medicine formula, has been used empirically for ovarian dysfunction, yet its molecular basis remains incompletely defined. This study aimed to delineate the mechanism by which GSW modulates inflammation-linked insulin signaling in a PCOS-relevant granulosa cell model under metabolic stress, with a focus on the TNF-α/PI3K/Akt axis. Methods: Network pharmacology based on serum-absorbed constituents identified by UPLC-MS/MS was integrated with Results: Network pharmacology highlighted TNF and PI3K/Akt signaling as key pathways. In the KGN metabolic stress model, GSW-medicated serum dose-dependently improved cell viability, reduced apoptosis, and attenuated inflammatory cytokine output (TNF-α and IL-6), accompanied by increased phosphorylation of PI3K and Akt. Recombinant TNF-α markedly diminished the protective and signaling-activating effects of GSW, supporting a TNF-α-linked mechanism. Embelin and nobiletin reproduced key anti-inflammatory and signaling effects, and their co-application produced an enhanced combined effect at the tested concentrations. Conclusion: These findings suggest that GSW mitigates PCOS-like granulosa cell dysfunction under metabolic stress by suppressing TNF-α-associated inflammatory signaling, thereby relieving inhibition of the PI3K/Akt pathway. Given the
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