Uncovering the mechanism of Jueyin granules in the treatment of psoriasis using network pharmacology

Authors Kuai, Le; Song, Jian-kun; Zhang, Ruo-xi; Xing, Meng; Luo, Ying; Ru, Yi; Ding, Xiao-jie; Liu, Liu; Lu, Yi; Sun, Xiao-ying; Nian, Hua; Li, Xin; Li, Bin

Journal JOURNAL OF ETHNOPHARMACOLOGY , NOV 15 2020,:262

DOI 10.1016/j.jep.2020.113214 PubMed 32736045

Abstract Ethnopharmacological relevance: Our clinical practice demonstrated that Jueyin granules (JYG) benefit patients with mild to moderate psoriasis vulgaris without apparent adverse effects. JYG have been shown to inhibit epidermal proliferation in an imiquimod (IMQ)-induced psoriasis-like mouse model, as well as keratinocyte proliferation. Moreover, JYG causes no acute or chronic toxicity in animal models. However, its related molecular mechanism has still not been elucidated.Aim of the study: To assess the mechanism of JYG against psoriasis. Materials and methods: This study combined network pharmacology analysis with experiments to investigate the mechanism of JYG against psoriasis. First, the molecular docking technology was used to construct the network of medicinal materials-core active plant ingredients-core targets and identify possible drug targets. Next, highperformance liquid chromatography (HPLC) was used for quality control of JYG. Finally, a mice model of psoriasis was used to further verify the effects of JYG.Results: (1) Molecular docking analysis of network pharmacology revealed that the therapeutic effects of JYG on psoriasis might be achieved through Vitamin D Receptor (VDR) effects. (2) The concentrations of chlorogenic acid and paeoniflorin were determined using HPLC to establish quality control of JYG. (3) JYG ameliorated pathological characteristics that included in vivo reductions in erythema, scale, and infiltration scores of back and ear lesions in IMQ-induced psoriasis-like mice. Moreover, a reduced number of PCNA-positive and Ki67-positive cells were observed in the epidermis of JYG-treated lesions. JYG also reduced inflammation (interleukin (IL)-17, IL-23) in the peripheral blood of IMQ-induced psoriasis-like mice. As expected, JYG was found to upregulate VDR expression and downregulate p-STAT3 expression in the IMQ group, which may contribute to its mechanism against psoriasis.Conclusion: Overall, this study clarifies the mechanism of JYG against psoriasis and provides evidence to support its clinical use.