Anacardic acid inhibits the proliferation and inflammation of HaCaT cells induced by TNF-α via the regulation of NF-κB pathway

Purpose: To determine the effect of anacardic acid on HaCaT cells invitro and to elucidate its molecular action .Methods:HaCaT cells were incubated in varying concentrations of anacardic acid (10 to 50 mu M). To model psoriasis, the cells were treated with tumor necrosis factor-alpha (TNF-alpha); cell viability was gauged by CCK-8assay. Apoptosis was determined, and Bcl-2, Bax, p65,p-p65, p-I kappa B alpha and I kappa B alpha by Western blot. Levels of pro-inflammatory cytokines were evaluated by enzyme-linked immunosorbent assay (ELISA). Results: Anacardic acid resulted in reduced HaCaT cell viability and increased cell apoptosis in a concentration-dependent manner (p < 0.05). It also curtailed TNF-alpha-mediated inflammatory responses and downregulated the NF-kappa B signaling axis. Conclusion: The results indicate that anacardic acid impedes HaCaT cell growth and inflammatory cytokine production by interferingwith NF-kappa B signal transduction, and may influence the development of AA-based therapies for psoriasis