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Abstract
Psoriasis is a chronic inflammatory skin disorder with a pathogenesis involving the interleukin-23/interleukin-17 axis. Salvianolic acid B exerts several pharmacological effects, such as antioxidation, anti-inflammation, and antitumor effects. The anti-psoriatic effects of salvianolic acid B have not been reported. In this study, we aimed to determine the optimum vehicle for salvianolic acid B, investigate its therapeutic effect on psoriatic-like skin conditions, and explore its underlying mechanisms of action. BALB/c mice were administered topical imiquimod to induce psoriasis-like skin and were then randomly assigned to control, vehicle control, salvianolic acid B in vehicles, and 0.25% desoximetasone ointment treatment groups. Barrier function, cytokine expression, histology assessment, and disease severity were evaluated. The results showed that salvianolic acid B-containing microemulsion alleviated disease severity, reduced acanthosis, and inhibited interleukin-23/interleukin-17 (IL-23/IL-17) cytokines, epidermal proliferation, and increased skin hydration. Our study suggests that salvianolic acid B represents a possible new therapeutic drug for the treatment of psoriasis. In addition, such formulation could obtain high therapeutic efficacy in addition to providing sufficient hydration for dry skin.
Highlights
Psoriasis is a common chronic inflammatory skin disease, with histopathological features of epidermal hyperproliferation, abnormal keratinocyte differentiation, angiogenesis with blood vessel dilatation, and excess T helper 1 cell (Th-1) and T helper 17 cell (Th-17) lymphocyte infiltration [1,2,3]
To select the suitable formulation, the skin irritation study was conducted by an IMQ-induced psoriasis-like dermatitis model
B showed non-inferior therapeutic effects compared with desoximetasone for IMQ-induced psoriasis treatment
Summary
Psoriasis is a common chronic inflammatory skin disease, with histopathological features of epidermal hyperproliferation, abnormal keratinocyte differentiation, angiogenesis with blood vessel dilatation, and excess T helper 1 cell (Th-1) and T helper 17 cell (Th-17) lymphocyte infiltration [1,2,3]. IL-23, secreted by dermal dendritic cells, can induce Th17 lymphocyte differentiation with a subsequent release of proinflammatory cytokines on keratinocytes, leading to epidermal hyperplasia and parakeratosis [3,4]. Dermatology studies have reported that Sal. B had pro-angiogenesis, antiapoptosis, and antioxidative stress effects by stimulating autophagy that enhances the survival of skin flaps and wound healing [10,11,12]. The effect of Sal. B on psoriasis has not yet been reported
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