Apigenin ameliorates imiquimod-induced psoriasis in C57BL/6J mice by inactivating STAT3 and NF-κB

Psoriasis is a chronic autoimmune disease featured by patches on the skin. It caused malfunction of immune cells and keratinocytes with inflammation as one its key features. Apigenin (API) natural flavonoid anti-inflammatory immunoregulatory properties. Therefore, we speculated that API can ameliorate psoriasis, determined effect development psoriasis using imiquimod (IMQ)-induced mouse model. Our results showed attenuated IMQ-induced phenotypic changes, such erythema, scaling epidermal thickening, improved splenic hyperplasia. Abnormal differentiation was restored in API-treated mice. Mechanistically, revealed regulator signal transducer activator transcription 3 (STAT3). regulated responses reducing interleukin-23 (IL-23)/STAT3/IL-17A axis. Moreover, it suppressed IMQ-caused cell hyperproliferation inactivating STAT3 through regulation extracellular signal-regulated kinase 1/2 nuclear factor-κB (NF-κB) pathway. Furthermore, reduced expression inflammatory cytokines inactivation NF-κB. Taken together, our study demonstrates may be considered strategy for treatment.