Mechanism of quercetin in the treatment of oral ulcer through network pharmacology and experimental validation.

Oral ulcer is one of the most prevalent oral disorders, and is characterized by a high tendency to recur. Quercetin, a naturally occurring flavonoid, possesses antioxidant and anti-inflammatory properties. However, the mechanisms underlying the therapeutic effects against oral ulcer remain unclear. To address this issue, the present study employed an integrated approach combining network pharmacology prediction and in vivo experimental validation to investigate this issue. Network pharmacology analyses identified 167 intersecting targets between quercetin and oral ulcer. Molecular docking revealed favorable binding affinities of quercetin for multiple core targets. In vivo studies using a rat model of oral ulcer demonstrated that quercetin significantly reduced the ulcer area, ameliorated ulcer severity, decreased the serum levels of pro-inflammatory cytokines, and downregulated the expression of phosphorylated phosphoinositide 3-kinase (p-PI3K) and phosphorylated protein kinase B (p-Akt). Collectively, these findings suggest that quercetin may exert its therapeutic effects against oral ulcer through modulation of the phosphoinositide 3-kinase (PI3K)-protein kinase B (Akt) signaling pathway, thereby providing experimental evidence to support its potential clinical application.