Exploring the therapeutic potential of syringaldehyde in imiquimod-induced psoriasis model in mice via NF-κB pathway inhibition.

Abstract

Psoriasis is characterized by increased levels of pro-inflammatory cytokines, including TNF-α, IL-1β, IL-17A, and NF-κB, as well as keratinocyte hyperproliferation and epidermal thickening. Its pathophysiology is significantly influenced by oxidative stress and abnormal activation of redox-sensitive signaling pathways, such as NF-κB and MAPK. The present study examined the potential of Syringaldehyde (SYD) in the imiquimod (IMQ) induced psoriasis model. Psoriasis Area Severity Index (PASI) scores, back skin thickness, and spleen hypertrophy decreased at dose levels of SYD 25, 50, and 100 mg/kg. Furthermore, a significant reduction in PASI scores following SYD administration indicated a marked improvement in the disease severity and lesion morphology. High-affinity binding of SYD to NF-κB (PDB ID: 4KIK; -34.76 kcal/mol) and MAPK (PDB ID: 1A9U; -32.87 kcal/mol) was found by molecular docking, indicating interference with nuclear translocation and phosphorylation processes. The treatment groups 50 mg/kg and 100 mg/kg indicated restoration of normal histological features. The biochemical evaluation showed decrease in NF-κB, IL-1β, TNF-α, and IL-17 on treatment with SYD. Thus, SYD appears to be a potential therapeutic option for psoriasis, but additional research is needed to confirm its efficacy and safety.