Analysis of a novel high-power low-temperature plasma indicates treatment of psoriasis through inhibition of the NF-κB pathway and Th17/IL-23 cell axis.

This study aims to evaluate the therapeutic efficacy and potential underlying mechanisms of a novel high-power low-temperature plasma (hLTP) therapy for treatment of psoriasis. Imiquimod (IMQ)-induced rat psoriasis model was used to evaluate the therapeutic efficacy of hLTP. Potential mechanisms were explored using bioinformatics analysis and molecular biology validation based on transcriptomic data. hLTP treatment alleviated IMQ-induced psoriasis as evidenced by a significantly reduced psoriasis area and severity index scores (PASI), and pathological changes. Based on the transcriptomic data, the differential expressed genes (DEGs) positively or negatively related to the hLTP treatment was identified and bioinformatics analysis was further performed. The results of the verification experiment indicate that hLTP treatment significantly elevated nitric oxide (NO) levels and FKBP5 expression in psoriasis, which was associated with inhibition of the NF-κBpathway, as indicated by reduced p-IKK/IKK and p-P65/P65 ratios. Apoptosis was suppressed, evidenced by a decreased cleaved-caspase3/caspase3 ratio and lower self-DNA levels. Antioxidant capacity was enhanced, shown by increased glutathione (GSH) levels, while the inflammatory response was mitigated with reduced cathelicidin (LL-37) levels. These effects resulted in reduced psoriasis-related pro-inflammatory cytokines (IL-23, IL-6, and TGF-β) from dendritic cells and macrophages, preventing Th17 cell differentiation and suppressing it related cytokines (IL-17 A, IL-22, IL-17F, TNF-α). Consequently, the Th17/IL-23 cell axis was disrupted under hLTP treatment.This is a novel study that provides conclusive data demonstrating that hLTP exerts significant therapeutic effects on psoriasis through its anti-inflammatory, antioxidant, and anti-apoptotic effects by significantly up-regulating NO and FKBP5, while inhibiting NF-κB pathway and Th17/IL-23 cell axis.