Inhibitory effect of apigenin on AK23-induced desmoglein3 depletion in HaCaT cell model of pemphigus vulgaris via suppression of p38 MAPK phosphorylation

• AK23 treated-HaCaT cells exhibited stronger intercellular adhesion when incubated with apigenin. • Apigenin prevented the AK23-mediated disappearance of cell-surface-localized Dsg3. • Apigenin inhibited the AK23-induced p38 MAPK phosphorylation and increased Dsg3 protein expression. • Apigenin could be useful as a functional natural food material to ameliorate PV. This study aimed to investigate the effect of apigenin, a flavonoid widely distributed in plants, on AK23-induced desmoglein3 (Dsg3) depletion in pemphigus vulgaris (PV) model using HaCaT cells. Dispase-based dissociation assay showed that the number of cell fragments, which increased compared to the control group due to AK23 treatment, dramatically decreased when HaCaT cells were incubated with AK23 and apigenin. The continuous linear fluorescence intensity of Dsg3 between cells was decreased in the AK23 group, but the treatment of apigenin recovered the fluorescent distribution of Dsg3. Moreover, the addition of apigenin up-regulated the Dsg3 protein expression in AK23-treated HaCaT cells. The phosphorylation level of p38 mitogen-activated protein kinase (MAPK) induced by the AK23 was down-regulated by apigenin. In conclusion, apigenin attenuated AK23-mediated Dsg3 depletion by suppressing the p38 pathway in the PV cell model. Therefore, apigenin could be a functional food material for ameliorating PV.