ArticleTranslational andrology and urology2025
7,8-dihydroxyflavone attenuates NIH IIIA subtype chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) via TrkB/AKT/SIRT3 signaling activation.
Article in Translational andrology and urology, 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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Abstract
Background: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) represents a prevalent urological disorder characterized by an unfavorable prognosis. Accumulating evidence indicates that suppression of excessive reactive oxygen species (ROS) generation significantly ameliorates its inflammatory manifestations. 7,8-dihydroxyflavone (7,8-DHF), a specific TrkB receptor agonist, which could subsequently trigger downstream signaling pathways such as AKT, demonstrates antioxidant and anti-inflammatory properties across diverse pathological conditions. Nevertheless, its potential therapeutic efficacy against CP/CPPS remains undefined. The aim of this study is to investigate the effects of 7,8-DHF on CP/CPPS and elucidate the underlying mechanisms involved, thereby providing fundamental experimental data for the clinical research of pharmacological interventions for CP/CPPS. Methods: CP/CPPS rat model was established via intraprostatic injection of complete Freund's adjuvant (CFA). Utilizing this experimental prostatitis model, we evaluated the effects of 7,8-DHF on prostate index, mechanical hyperalgesia, prostate histopathology, oxidative stress markers, pro-inflammatory cytokine expression, and immune cell infiltration. Molecular analyses further assessed TrkB/AKT/SIRT3 signaling pathways in RWPE-1 cells. We have cultivated human prostate epithelial cells RWPE-1. Results: At the animal level, 7,8-DHF administration concurrently suppressed CFA-induced elevations in prostate index, mechanical hyperalgesia, inflammatory cell infiltration, and pro-inflammatory cytokine levels, while significantly ameliorating histological damage. At the cellular level, 7,8-DHF attenuates LPS-induced cellular damage and inflammatory responses through mechanisms involving the activation of TrkB/AKT/SIRT3 signaling, augmented antioxidant enzyme activity, mitigated ROS overproduction and pro-inflammatory mediator expression, thus disrupting the "oxidative stress-inflammation" vicious cycle. Conclusions: This study identifies 7,8-DHF as a novel therapeutic agent for CP/CPPS, and the potential role of the TrkB/AKT/SIRT3 pathway in the improvement of CP/CPPS by 7,8-DHF, thereby establishing a foundational basis for future CP/CPPS therapeutics.
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