ArticleClinical, cosmetic and investigational dermatology2026
Network Pharmacology and Animal Experimental Validation on the Therapeutic Mechanisms of
Article in Clinical, cosmetic and investigational dermatology, 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
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Psoriasis is a chronic immune-mediated inflammatory skin disorder characterized by excessive keratinocyte proliferation and persistent inflammation. Its multifactorial pathogenesis involves complex inflammatory mediators and signaling pathways. Current treatments remain limited by high recurrence and adverse effects, highlighting the need for safe and effective natural bioactive compounds for psoriasis prevention and management. In addition, cyclin B1 (CCNB1) has been reported as a hub gene associated with psoriasis; however, its mechanism of action remains unclear. Objective: To elucidate the potential therapeutic mechanisms of a bioactive extract derived from Methods: A psoriasis-like mouse model was established using imiquimod (IMQ) in mice as the study subjects. The anti-psoriatic effect of PCE10 was assessed using the Psoriasis Area and Severity Index (PASI), histopathological examination, and inflammatory cytokine assays. Network pharmacology combined with machine learning algorithms was employed to identify psoriasis-associated target genes potentially regulated by PCE10. Molecular docking were subsequently performed to predict the binding interactions between candidate bioactive compounds and key molecular targets. Results: Network pharmacology identified 67 psoriasis-related targets, with 23 hub genes detected in the protein-protein interaction network. Enrichment analyses indicated involvement in inflammatory regulation and TNF, NF-κB, and p53 pathways. Machine learning identified CCNB1 as a key psoriasis-associated gene. Molecular docking indicated interactions between p53 and the bioactive compounds of PCE10. In vivo, PCE10 alleviated IMQ-induced psoriasis-like dermatitis and reduced epidermal hyperplasia, decreasing serum levels of IL-23, IL-17A, and TNF-α. Mechanistically, PCE10 suppressed keratinocyte proliferation by modulating the p53/CCNB1 axis. Conclusion: PCE10 may exert anti-psoriatic effects through modulation of p53/CCNB1 regulatory axis. Nevertheless, this study is mainly based on an IMQ-induced mouse model and is not supported by validation in human psoriatic skin tissues or clinical specimens. Additional translational studies are required to establish its clinical applicability.
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.