ArticleReproductive sciences (Thousand Oaks, Calif.)2025
Kuntai Capsules Improve Premature Ovarian Failure by Regulating AMPK-Mediated Autophagy.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2025. 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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Who cites it
1 citing paper in PubMed.
- Relationship between different modes of death and premature ovarian insufficiency: a literature review.Apoptosis : an international journal on programmed cell death · 2026Review
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5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundPremature ovarian failure (POF) is a gynecological endocrine disorder with current treatments having limitations. Kuntai capsule (KTC), a traditional Chinese medicine formulation, is thought to be beneficial for POF, but its mechanism is unclear. Network pharmacology can help explore drug mechanisms.
methodsA POF rat model was established using cyclophosphamide (CTX). Rats received low-dose KTC (0.6 g/kg/d), high-dose KTC (1.8 g/kg/d), or dehydroepiandrosterone (DHEA, positive control). Ovarian function was evaluated via histopathology, hormone assays (ELISA), apoptosis (TUNEL/flow cytometry), autophagy markers (Western blot), and network pharmacology.
resultsKTC treatment (especially high-dose) ameliorated POF in CTX-treated rats, as shown by increased ovarian weight, restored estrus cycle, and improved follicle development. The serum estradiol (E2), anti-mullerian hormone (AMH), and superoxide dismutase (SOD) levels increased, whereas the follicle-stimulating hormone (FSH), malondialdehyde (MDA), and reactive oxygen species (ROS) levels decreased following KTC treatment. KTC also alleviated ovarian cell apoptosis and autophagy, with higher-dose KTC being more effective. Network pharmacology predicted AMPK/mTOR pathway involvement. Western blot confirmed KTC activated the AMPK/mTOR signaling, downregulated autophagy markers (LC3B-II/I, Beclin1), and upregulated P62. Autophagy inhibition (via 3-MA) mirrored KTC effects, while mTOR blockade (rapamycin) reversed them.
conclusionsKTC ameliorates POF by inhibiting excessive ovarian autophagy through AMPK/mTOR pathway activation, providing a mechanistic basis for its clinical use.
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