关键词: 淫羊藿苷, 银屑病, PI3K-AKT信号通路, 血管增生

Abstract: Objective To explore the mechanism of icariin (ICA) in the treatment of psoriasis. Methods Thirty-six C57BL/6 mice were randomly divided into 6 groups with 6 in each: a blank(Ctrl) group, a model group, a positive control group treated with methotrexate, and experimental groups treated respectively with low, medium, and high doses of ICA. Ann imiquimod (IMQ)-induced psoriasis animal model was established. Methotrexate was given by intragastric administration at a concentration of 1 mg/kg. The animals in low, medium, and high dose ICA groups received intragastric administration of 0.4 mg/100 mL, 0.8 g/100 mL and 1.2 g/100 mL respectively. On day 6 of the experiment, dorsal skin samples were collected from all six groups of mice for Hematoxylin-Eosin (HE) staining microscopy. RT-qPCR was used to measure the inflammatory level of Il-6, Il-17a and Tnf-α in the mouse skin. Immunofluorescence double staining was employed to observe CD31 and VEGF level in the mouse skin. Western blot was used to detect the protein level of PI3K, AKT, p-PI3K, and p-AKT in the mouse skin. Results Compared with the model group, the high-dose ICA group significantly improved IMQ-induced skin thickening(P＜0.000 1) and reduced the PASI score in mice. The high-dose ICA group significantly decreased mRNA level of Tnf-α, Il-6 and Il-17a in the skin of psoriasis mice (P＜0.000 1) and reduced the level of CD31 and VEGF in the skin of psoriasis mice. Additionally, the high-dose ICA group reduced protein level of PI3K(P＜0.05), AKT(P＜0.05), p-PI3K (P＜0.05) and p-AKT (P＜0.01) in the mouse skin. Conclusions High-dose 1.2 g/100 mL ICA exhibits superior anti-psoriatic properties, with its mechanism potentially involving inhibition of PI3K-AKT-mediated angiogenesis.

Key words: icariin, psoriasis, PI3K-AKT signaling pathway, angiogenesis