Modulation of the KEAP1-NRF2 pathway by Erianin: A novel approach to reduce psoriasiform inflammation and inflammatory signaling.

Psoriasis is a chronic, immune-mediated skin condition marked by excessive cell growth and inflammation. Current therapies frequently have limitations, such as side effects and insufficient efficacy, emphasizing the need for safer, more effective options. Erianin (ERN), a naturally occurring bioactive molecule produced from Dendrobium chrysotoxum, has anti-inflammatory and antioxidant characteristics, although its therapeutic potential in psoriasis has not been fully investigated. The purpose of this investigation was to look into the protective benefits of ERN against psoriasis-like skin inflammation utilizing laboratory-based cell models and an imiquimod-induced psoriasis animal model. Human keratinocytes were subjected to pro-inflammatory cytokines in vitro to simulate psoriasis disease, and cell survival and proliferation were measured. In vivo, mice given ERN for 6 days demonstrated a significant decrease in skin thickness, inflammatory cell infiltration, and overall histopathological alterations. ERN reduced pro-inflammatory substances (IL-6, IL-17, IL-23, IL-1β), TNF-α, COX-2, and inducible nitric oxide synthase, while increasing anti-inflammatory cytokine IL-10 and antioxidant-related molecules. Additionally, ERN stimulated the Kelch-like ECH-associated protein 1- nuclear factor erythroid 2-related factor 2 signaling pathway, which is essential for cellular antioxidant defense. The results presented here demonstrate that ERN reduces psoriasis-like inflammation by modifying immunological responses and increasing antioxidant protection, pointing to its potential as a viable therapeutic agent for psoriasis treatment.