Chinese herbal medicine Jia Wei Jing Xie Yin (JWJXY) ameliorates psoriasis via suppressing the Th17 cell response

Background: Psoriasis is a chronic autoimmune disease. At present, it is very difficult to treat; however, clinical trials have shown that the traditional Chinese medicine (TCM) treatment of psoriasis has certain advantages. The Chinese herbal medicine Jia Wei Jing Xie Yin (JWJXY) has its origins in Jing Xie Yin, a medicine created by the TCM doctor Wu Jun. Previous studies have shown that JWJXY has good clinical efficacy for patients with blood-heat type psoriasis, but its mechanism is unknown. Methods: This paper aimed to further study the therapeutic effect and mechanism of JWJXY on an imiquimod (IMQ)-induced, psoriasis-like mouse model (0.4 mL, i.g., 6 days). The histopathological skin changes were observed by hematoxylin and eosin (HE) staining, the infiltration of cluster of differentiation 11B (CD11b) and cluster of differentiation 4 (CD4) cells was observed by immunohistochemistry, lymphocyte subsets were detected by flow cytometry, T helper (Th)17 cell expression was perceived by flow cytometry, and Th17 cell-related gene expression was detected by real-time quantitative polymerase chain reaction (qPCR). Results: JWJXY significantly reduced the skin thickness of the IMQ-induced model mouse. Compared with that in the vehicle group, the skin tissue of the mice in the JWJXY group showed significantly reduced infiltration of CD11b(+) and CD4(+) T cells. Flow cytometry results showed that JWJXY decreased the proportion of B220 and Th17 cells in the spleen tissue of the mice. There was no significant effect on the proportion of Thl or regulatory T cells (Treg) cells. Compared with that in the vehicle group, the skin tissue of the mice in the JWJXY group showed significantly decreased expression of interleukin-17A (IL-17A), IL-17F, retinoic acid receptor-related orphan receptor gamma t (ROR gamma t), IL-1 beta, interferon gamma (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) messenger RNA (mRNA). Conclusions: The study confirmed the therapeutic effect of JWJXY on psoriasis. Its mechanism of action might be to inhibit the Th17 cell response but not the Th1 and Treg response.