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

Abstract

Purpose: To determine the effect of anacardic acid on HaCaT cells in vitro and to elucidate its molecular action. Methods: HaCaT cells were incubated in varying concentrations of anacardic acid (10 to 50 μM). To model psoriasis, the cells were treated with tumor necrosis factor-α (TNF-α); cell viability was gauged by CCK-8 assay. Apoptosis was determined, and Bcl-2, Bax, p65, p-p65, p-IκBα and IκBα 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-α-mediated inflammatory responses and downregulated the NF-κB signaling axis. Conclusion: The results indicate that anacardic acid impedes HaCaT cell growth and inflammatory cytokine production by interfering with NF-κB signal transduction, and may influence the development of AA-based therapies for psoriasis.