Dihydroartemisinin targets fibroblast growth factor receptor 1 (FGFR1) to inhibit interleukin 17A (IL-17A)-induced hyperproliferation and inflammation of keratinocytes.

Psoriasis is a common chronic immune-mediated disease that often has a serious negative impact on the physical and mental health of patients. Dihydroartemisinin (DHA) is a drug with anti-fibrotic and anti-inflammatory effects that may be involved in the autoimmune regulation of immune diseases. However, the effects of DHA on psoriasis have not been reported comprehensively. Therefore, the aim of this study was to investigate the effect of DHA on abnormal proliferation and inflammation of epidermal keratinocyte cells in psoriasis and its mechanism of action. IL-17A-induced human epidermal keratin-forming cells (HaCaT) were used as a model. And after induction exposure to different concentrations of DHA, CCK-8, EDU staining, wound healing and Western blotting were performed to assess cell viability, proliferation, migration, differentiation and inflammatory factors, respectively. Subsequently, agonists of fibroblast growth factor receptor 1 (FGFR1) were added and the above experiments were repeated. The results showed that DHA obviously inhibited IL-17A-induced hyperproliferation, migration and expression of inflammatory factors in HaCaT cells. Furthermore, FGFR1 was highly expressed in IL-17A-induced HaCaT cells, and DHA inhibited its expression. However, the inhibitory effect of DHA on IL-17A-induced HaCaT cells was reversed after the addition of FGFR1 agonist. In conclusion, DHA could inhibit IL-17A-induced hyperproliferation and inflammation of keratinocytes by targeting FGFR1, which also provided a new target for the treatment of psoriasis.