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

银屑病 药理学 芍药苷 医学 红斑 伊米奎莫德 角质形成细胞 作用机理 化学 免疫学 高效液相色谱法 体外 生物化学 色谱法
作者
Le Kuai,Jiankun Song,Ruo-xi Zhang,Meng Xing,Ying Luo,Yi Ru,Xiaojie Ding,Liu Liu,Yi Lü,Xiaoying Sun,Hua Nian,Xin Li,Bin Li
出处
期刊:Journal of Ethnopharmacology [Elsevier]
卷期号:262: 113214-113214 被引量:20
标识
DOI:10.1016/j.jep.2020.113214
摘要

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. To assess the mechanism of JYG against psoriasis. 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, high-performance 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. (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. Overall, this study clarifies the mechanism of JYG against psoriasis and provides evidence to support its clinical use.
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