A study in mice showed that chelerythrine, a natural compound from the bark of Phellodendri Chinensis, can calm the skin inflammation and excess blood‑vessel growth that cause rosacea. It works by blocking several inflammation‑related pathways and by nudging immune cells toward a less aggressive state.

Rosacea is a chronic inflammatory skin condition marked by excessive M1 macrophage polarization and angiogenesis, resulting in erythema and tissue inflammation. Despite available treatments, many patients experience recurrent flare-ups. This study explores chelerythrine, a bioactive component of Phellodendri Chinensis Cortex, for its therapeutic potential in rosacea through modulation of NF-κB, p38 MAPK and STAT3 signaling, inflammation, and vascular regulation. Using an LL-37-induced rosacea-like mouse model, THP-1-derived M1 macrophages and HUVECs, chelerythrine's effects on macrophage polarization, cytokine expression, angiogenesis and pathway activation of NF-κB, p38 MAPK and STAT3 were evaluated. Chelerythrine significantly reduced epidermal thickness, inflammatory cell infiltration, and pro-inflammatory markers (TNF-α and IL-1β). It inhibited NF-κB, p38 MAPK and STAT3 activation and decreased M1 polarization markers, shifting towards an anti-inflammatory profile. Furthermore, chelerythrine reduced vascular density and VEGF expression, impairing angiogenesis-related behaviors in HUVECs. These findings suggest that chelerythrine holds promise as a treatment for rosacea by mitigating inflammation and angiogenesis through targeted multiple pathways and macrophage modulation.