当归多糖对哮喘小鼠模型氧化应激与炎症反应的影响

The effects of angelica polysaccharide on oxidative stress and inflammation in asthmatic mouse model

目的探讨当归多糖对哮喘幼鼠模型氧化应激损伤与炎症反应的影响及可能机制。方法将45只BALB/c幼鼠随机分为对照组(Control)、模型组(Model)与当归多糖组(ASP),每组15只,卵蛋白致敏方法建立支气管哮喘幼鼠模型。收集肺泡灌洗液(BALF)并进行细胞计数;HE染色观察气道组织病理学改变;ELISA方法检测各组幼鼠BALF中白介素-1β(IL-1β)、白介素-4(IL-4)和肿瘤坏死因子α(TNF-α)的表达水平;ELISA方法检测各组幼鼠肺组织超氧化物歧化酶(SOD)和丙二醛(MDA)水平;Western blot方法检测幼鼠肺组织β-连环蛋白(β-catenin)与糖原合成酶激酶-3β(GSK-3β)的表达。结果给予当归多糖预处理能够明显降低哮喘幼鼠BALF中细胞总数及嗜酸性粒细胞数,降低肺组织炎症细胞浸润,降低哮喘幼鼠血清炎性因子IL-1β、IL-4和TNF-α的含量以及肺组织MDA含量,上调SOD含量,降低哮喘幼鼠肺组织β-catenin的表达,上调GSK-3β的表达(P<0.05)。结论当归多糖通过抑制wnt/β-catenin信号通路减轻哮喘幼鼠的氧化应激损伤与炎症反应。

Objective To investigate the effects of angelica polysaccharide on oxidative stress injury and inflammation in asthmatic young mice and its possible mechanism.Methods 45 female BALB/c mice were randomly divided into control group,model group and angelica polysaccharide group(ASP),with 15 mice in each group.A bronchial asthma model was established by ovalbu min sensitization.Bronchoalveolar lavage fluid(BALF)was collected and cell counts were performed.Histopathological changes of airway was observed by HE staining.The expressions of interleukin-1β(IL-1β),interleukin-4(IL-4)and tumor necrosis factor-α(TNF-α)in BALF were deter mined by ELISA.The levels of superoxide dismutase(SOD)and malondialdehyde(MDA)in lung tissue were deter mined by ELISA.The expressions ofβ-catenin(β-Catenin)and glycogen synthase kinase-3β(GSK-3β)in lung tissues of young mice were detected by Western blot.Results Pretreatment with angelica polysaccharide could significantly reduce the total number of cells and eosinophils in BALF of asthmatic young mice,reduce the infiltration of inflammatory cells in lung tissue,reduce the contents of IL-1β,IL-4 and TNF-αin serum of asthmatic young mice,reduce the content of MDA,increase the content of SOD in lung tissues of asthmatic young mice,and down-regulated the expression ofβ-catenin,up-regulated the expression of GSK-3βin lung tissue of asthmatic young mice(P<0.05).Conclusion Angelica polysaccharide alleviates oxidative stress damage and inflammation in asthmatic young mice by inhibiting wnt/β-catenin signaling pathway.