Network Pharmacology and Animal Experimental Validation on the Therapeutic Mechanisms of Prunus cerasifera Extract in Psoriasis.

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 Prunus cerasifera fruit powder (PCE10) by integrating network pharmacology and animal experimental validation.

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.