ArticleFrontiers in pharmacology2026
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Polycystic ovary syndrome (PCOS) is one of the most common endocrine and metabolic disorders affecting women of reproductive age. Methods: A dehydroepiandrosterone (DHEA)-induced mouse model of PCOS was established to evaluate the effects of DOP. Estrous cyclicity, ovarian histopathology, serum hormone levels, RT-qPCR, and Western blot analyses were performed to assess reproductive function, endocrine changes, and MAPK/ERK-related signaling. Results: DOP treatment restored estrous cyclicity, improved ovarian morphology, and partially normalized serum luteinizing hormone, follicle-stimulating hormone, and testosterone levels. In addition, DOP reduced ERK1/2 phosphorylation and downregulated the expression of CYP17A1 and CYP19A1. Conclusion: DOP ameliorated reproductive and endocrine abnormalities in a DHEA-induced mouse model of PCOS. The findings suggest that modulation of MAPK/ERK signaling may contribute to the biological effects of DOP, although further mechanistic studies are required to establish causal relationships.
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Registered trials
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