Dihydrotanshinone l alleviates psoriasis-like skin lesion via suppressing STAT3 signaling and DCs-Th17 responses.

Skin psoriasis involves the activation of skin dendritic cells (DCs) by external triggers. Activated DCs then secrete interleukin 23 (IL-23), which acts as a connector between innate and adaptive immunity and promotes the differentiation of T helper 17 (Th17) cells. This process leads to an elevated production of interleukin 17 (IL-17) and excessive keratinocyte production, creating an autoimmune loop in the development of psoriasis. Dihydrotanshinone 1 (DIH), a flavonoid recognized for its antitumor effects, was assessed for its impact on imiquimod (IMQ)-induced psoriatic plaques in mice. In this investigation, our team used IMQ-induced mouse models to study how DIH affects keratinocytes and skin immunity. At first, we noticed that psoriasis-like lesions were significantly more severe in mice treated with DIH. However, after giving DIH to IMQ-induced mice, we observed a reduction in hyperproliferative keratinocytes, cytokine release, and the accumulation of DCs and Th17 cells. Further exploration showed that DIH relieved psoriasis-like skin conditions and inhibited the abnormal proliferation of HaCaT cells and Th17 cell differentiation. In particular, we found that DIH achieved these outcomes by modulating the STAT3 signaling pathway, which in turn suppressed DCs/Th17 cell responses and keratinocyte proliferation. Hence, DIH may affect the recruitment and function of immune cells in the skin and alter keratinocyte proliferation and differentiation in the context of psoriasis.