Objective: To investigate the efficacy of horse oil on lipopolysaccharide (LPS)-induced inflammation in human keratinocytes.
Methods: Western blot analysis was performed to measure the expression of cyclooxygenase-2 (COX-2) and IκBα. ELISA was used to analyze prostaglandin E2 (PGE2) levels.
Results: Horse oil decreased LPS-induced COX-2 and PGE2 levels in a dose-dependent manner. Nuclear factor-kappa B (NF-κB) plays a key role in the expression of inflammatory cytokines and mediators. Therefore, we investigated the influence of horse oil on the NF-κB signaling pathways. Horse oil inhibited translocation of NF-κB from the cytosol to the nucleus. Furthermore, LPS-induced degradation of IκBα was recovered by horse oil. The activation of p38 mitogen-activated protein kinase (MAPK) reportedly induces degradation of IκBα In agreement with this, LPS activated p38 MAPK and caused IκBα degradation. Conversely, horse oil inhibited LPS-induced p38 MAPK activation and IκBα degradation. In addition, a specific p38 MAPK inhibitor, SB203580, blocked IκBα degradation.
Conclusion: Horse oil decreased COX-2 and PGE2 by inhibiting p38 MAPK activation, IκBα degradation, and the translocation of NF-κB.
Keywords: Cyclooxygenase 2; Dinoprostone; Horse oil; Inflammation; Ipopolysaccharide; Keratinocyte; Mitogen-activated protein kinase; NF-kappa B.