Inflammatory and Immunomodulatory Effects of Tripterygium wilfordii Multiglycoside in Mouse Models of Psoriasis Keratinocytes

Objective: To determine the role of Tripterygium wilfordii multiglycoside (TGW) in the treatment of psoriatic dermatitis from a cellular immunological perspective. Methods: Mouse models of psoriatic dermatitis were established by imiquimod (IMQ). Twelve male BALB/c mice were assigned to IMQ or IMQ+TGW groups according to a random number table. Histopathological changes in vivo were assessed by hematoxylin and eosin staining. Ratios of immune cells and cytokines in mice, as well as PAM212 cell proliferation in vitro were assessed by fl ow cytometry. Pro-inflammatory cytokine expression was determined using reverse transcription quantitative polymerase chain reaction. Results: TGW significantly ameliorated the severity of IMQ-induced psoriasis-like mouse skin lesions and restrained the activation of CD45+ cells, neutrophils and T lymphocytes (all P<0.01). Moreover, TGW significantly attenuated keratinocytes (KCs) proliferation and downregulated the mRNA levels of infl ammatory cytokines including interleukin (IL)-17A, IL-23, tumor necrosis factor a, and chemokine (C-X-C motif) ligand 1 (P <0.01 or P<0.05). Furthermore, it reduced the number of ?dT17 cells in skin lesion of mice and draining lymph nodes (P<0.01). Conclusions: TGW improved psoriasis-like infl ammation by inhibiting KCs proliferation, as well as the associated immune cells and cytokine expression. It inhibited IL-17 secretion from ?dT cells, which improved the immune-infl ammatory microenvironment of psoriasis.

Automated summary

Tripterygium wilfordii multiglycoside (TGW) improves psoriasis-like inflammation by inhibiting keratinocytes proliferation and regulating immune cells and cytokine expression. It also reduces the number of γδT17 cells in skin lesions and draining lymph nodes.