Exploring the mechanism of Panax notoginseng injection in the treatment of skin wound based on network pharmacology and experimental verification.

Prolonged healing of skin wounds remains a major clinical challenge. This study employed network pharmacology combined with in vivo experimental validation to investigate the mechanisms of Panax notoginseng (PN) in treating skin wounds. Network pharmacology identified 156 targets and 115 signaling pathways, with top core targets (TNF, IL-6, IL-10) enriched in NF-κB, MAPK, and JAK-STAT pathways. Molecular docking showed favorable binding affinities between PN components (Ginsenoside Rb₁, Rd, Re, Rg₁, Notoginsenoside R₁) and key target proteins. In vivo, 48 SD rats were randomly divided into a PN group and a control group with a full-thickness skin excision model. The PN group showed significantly smaller wound areas at days 4 and 7 (P < 0.05), with reduced inflammatory cell infiltration and enhanced fibroblast proliferation at day 7. qRT-PCR and ELISA demonstrated that TNF-α was significantly lower in the PN group at days 4 and 7 (P < 0.01), IL-6 was lower at all time points (P < 0.01), and IL-10 was lower at days 1 and 7 (P < 0.01). These findings suggest that PN modulates the inflammatory cytokine network (TNF-α, IL-6, IL-10) in a time-dependent manner, consistent with the regulation of the "inflammation initiation → repair transition" temporal sequence, representing a promising natural agent for regulating the inflammatory phase of skin wound healing.