ArticleBiology direct2026
Cepharanthine alleviated chronic prostatitis/chronic pelvic pain syndrome by activating Nrf2 and inhibiting the NF-κB pathway.
Article in Biology direct, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
1 citing paper in PubMed.
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
backgroundChronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common disorder impacting the genitourinary system of adult males, primarily driven by pathogenic mechanisms involving immune and inflammatory mediators, immune cells and molecules, oxidative stress, and apoptosis. Cepharanthine (CEP), a bisbenzylisoquinoline alkaloid, exhibits properties such as immunomodulatory, antioxidant, anti-inflammatory, and antitumor activities. Nevertheless, the effects of CEP on CP/CPPS and its underlying mechanisms remain insufficiently characterized.
methodsTwo experimental models were developed, one utilizing experimental autoimmune prostatitis (EAP) mouse models and the other employing LPS-induced RWPE-1 cells. The pivotal role of Nrf2 was investigated using Nrf2 knockout mice and the Nrf2 inhibitor ML385.
resultsTreatment with CEP reduced prostate inflammation scores, alleviated tactile sensitization of the pelvic region in EAP mice, improved pathological damage in prostate tissues, and inhibited the upregulation of systemic and localized pain and pro-inflammatory mediators in the prostate. Furthermore, CEP treatment was shown to inhibit oxidative stress, ameliorate mitochondrial dysfunction, and suppress apoptosis. In vitro studies indicate that CEP treatment stabilizes Nrf2 protein levels by binding to the Nrf2 protein and inhibiting its ubiquitination-mediated degradation. Consequently, CEP treatment activates the Nrf2 signaling pathway, facilitates its nuclear translocation, and upregulates the expression of downstream target proteins, such as HO-1 and NQO1. Concurrently, CEP suppresses the activation of the NF-κB pathway. Notably, the blockade of Nrf2 signaling negates the protective effects mediated by CEP.
conclusionsCEP inhibits the ubiquitination-mediated degradation of Nrf2 and exhibits potential to activate the Nrf2 pathway while concurrently inhibiting the NF-κB pathway, thereby alleviating CP/CPPS.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.