Eriodictyol inhibits the proliferation and inflammatory response in keratinocytes in psoriasis through inactivating DYRK1A-mediated endoplasmic reticulum stress

Our work is conducted to reveal the impacts of eriodictyol on psoriasis. CCK-8 and EdU assays measured HaCaT cell proliferation. ELISA detected the activities of inflammatory cytokines and chemokines. Western blot examined the expressions of proliferation-, inflammation- and ERS-associated proteins. Molecular docking predicted the binding affinity of eriodictyol to DYRK1A. RT-qPCR and Western blot analyzed DYRK1A expression. Eriodictyol inhibited the proliferation and inflammatory response in M5-challenged HaCaT cells. Eriodictyol targeted and down-regulated DYRK1A expression. DYRK1A overexpression abolished the impacts of eriodictyol on M5-stimulated HaCaT cells. Conclusively, eriodictyol might suppress ERS mediated by DYRK1A to elicit anti-psoriasis functions.