【摘要】 旨在揭示加味玉屏风多糖(JYP)调节免疫抑制的作用机制，为其临床应用提供理论依据。利用网络药理学分析JYP调节免疫抑制疾病的“成分-靶标-通路”分子机制，通过RAW264.7细胞和环磷酰胺诱导的免疫抑制小鼠模型进行体内外试验验证。网络药理学分析显示，JYP与免疫抑制疾病存在49个共同靶点，主要富集于PI3K/AKT信号通路和氧化应激反应。体外试验表明，31.25～125μg/mL浓度内的JYP可显著增加上清液中NO含量(P<0.05),上调过氧化氢酶(CAT)和超氧化物歧化酶(SOD)的基因表达。动物试验证实，JYP干预显著提升小鼠回肠组织中PI3K、AKT和Nrf2蛋白表达(P<0.05),同时抑制Keap1蛋白表达。综上所述，JYP能够通过激活Keap1/Nrf2抗氧化防御通路和PI3K/Akt信号通路，发挥抗氧化与免疫调节的双重效应。更多还原

【Abstract】 The aim was to elucidate the underlying mechanisms of Jiawei Yupingfeng polysaccharides(JYP) in regulating immunesuppression, and provide a theoretical basis for its clinical application.Network pharmacology was employed to analyze the "component-target-pathway" molecular mechanism of JYP in immunosuppressive diseases, followed by in vitro validation using RAW264.7 macrophages and in vivo verification in cyclophosphamide-induced immunosuppressed mice.Network pharmacological analysis identified 49 common targets between JYP and immunosuppressive diseases, which were significantly enriched in the PI3K/AKT signaling pathway and oxidative stress response.in vitro,experiments demonstrated that JYP at concentrations of 31.25-125 μg/mL significantly increased nitric oxide(NO) production in cell supernatants(P<0.05),and upregulated the mRNA expression of catalase(CAT) and superoxide dismutase(SOD).In vivo studies confirmed that JYP intervention significantly enhanced the protein expression of PI3K,AKT,and Nrf2 in mouse ileal tissues(P<0.05),while reducing Keap1 protein expression.Taken together, JYP exerted dual effects of antioxidation and immunomodulation by activating the Keap1/Nrf2 antioxidant defense pathway and the PI3K/Akt signaling pathway.更多还原