Exploring the mechanism of α-Bisabolol in the treatment of psoriasis based on network pharmacology and experimental validation.

Abstract

This study aims to evaluate the effects of α-Bisabolol in the treatment of psoriasis both in vivo and in vitro, and to elucidate its mechanism of action. We used network pharmacology to explore the potential active components and targets of α-Bisabolol in the treatment of psoriasis. Psoriasis-like models were induced in mice or keratinocytes using imiquimod (IMQ) or tumor necrosis factor-α (TNF-α). The results indicated that α-Bisabolol shares 133 potential genes with psoriasis, and pathway enrichment analysis showed that the PI3K/AKT and nuclear factor κB (NF-κB) signaling pathways are considered key pathways. In vivo experiments showed that α-Bisabolol reduced epidermal thickening, inflammatory cell infiltration, and histological psoriasis-like lesions in IMQ-induced mice (P<0.05, P<0.01). α-Bisabolol inhibited the elevation of inflammatory cytokines (including interleukin-6(IL-6), interleukin-1β(IL-1β), interleukin-17A(IL-17A), interleukin-23(IL-23) and tumor necrosis factor-α (TNF-α)) in skin lesions of mice and TNF-α-treated HaCat cells (P<0.05, P<0.01). Mechanistically, α-Bisabolol inhibited the phosphorylation of PI3K/AKT (PI3K and AKT) and NF-κB (IκB and p65) signaling pathways activated by IMQ (P<0.05, P<0.01). Similar changes were detected in TNF-α-treated HaCaT cells. This suggests that α-Bisabolol may inhibit inflammation in TNF-α-treated keratinocytes and psoriasis mice through the PI3K/AKT and NF-κB pathways, providing a new theoretical basis for clinical application in the treatment of psoriasis.