ArticleFrontiers in pharmacology2025
Nobiletin mitigates benign prostatic hyperplasia by suppressing prostate cell proliferation through regulation of cell cycle progression, signaling pathways, transcription factor activity, and the androgen-signaling axis.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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12 authors.
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Abstract
Background and aim: Benign prostatic hyperplasia (BPH) involves androgen-driven proliferation with reduced apoptosis. Current 5α-reductase inhibitors can cause adverse effects, motivating safer options. We evaluated whether nobiletin, a polymethoxyflavonoid, mitigates BPH features. Methodology: Results: Nobiletin induced G0/G1 phase cell cycle arrest by suppressing cyclin D1, cyclin E, and cyclin-dependent kinase 2 (CDK2), while elevating p21 and p27 expression. Expression of 5α-reductase, androgen receptor (AR), fibroblast growth factor (FGF), epidermal growth factor (EGF), and B-cell lymphoma 2 (Bcl-2) was reduced, whereas Bcl-2-associated X protein (Bax) was increased. Nobiletin modulated phosphorylation of c-Jun N-terminal kinase (JNK) and p38 and suppression of protein kinase B (AKT) phosphorylation. Nobiletin reduced nuclear factor kappa B (NF-κB) DNA-binding activity, which was dependent on JNK and p38. Conclusion: These results highlight the potential of nobiletin as a novel therapeutic option for BPH.
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