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目的建立葎草花粉粗浸液诱导的小鼠变态反应气管炎症动物模型。方法制备葎草花粉粗浸液,将40只清洁级雌性BALB/c小鼠按随机数字表法分为4组,每组10只。①空白对照组:PBS+氢氧化铝致敏激发;②低剂量组:100μg葎草粗浸液+氢氧化铝致敏激发;③中剂量组:200μg葎草粗浸液+氢氧化铝致敏激发;④高剂量组:300μg葎草粗浸液+氢氧化铝致敏激发。通过HE染色观察小鼠肺部炎症和黏液分泌,支气管肺泡灌洗液中细胞总数和细胞分类,酶联免疫吸附试验检测BALF,脾组织匀浆上清的IL-4、IFN-γ和血清抗原特异的抗体验证哮喘动物模型。结果随着抗原浓度的升高,肺部病理改变呈明显的变态反应炎症;高剂量组小鼠支气管肺泡灌洗液中的细胞总数为(210.75±78.80)×106/L、巨噬细胞数为(48.65±3.27)%、EOS数为(24.37±4.28)%、IL-4、血清抗原特异性IgE抗体、IgG1抗体明显高于空白对照组(P<0.05);支气管肺泡灌洗液﹑脾组织匀浆上清的IFN-γ较空白对照组下降(P<0.05)。结论葎草花粉成功构建小鼠变态反应气道炎症动物模型。
Objective To establish a mouse model of allergic tracheal inflammation induced by Humulus pollens crude extract. Methods Polysaccharide crude extract was prepared and divided into 4 groups of 10 female BALB / c mice of clean grade according to random number table. ① blank control group: sensitized by PBS + aluminum hydroxide; ② low dose group: 100μg Rhizoma Chuanxica crude extract + aluminum hydroxide sensitized; ③ medium dose group: 200μg Rhizoma Chuancao crude extract + aluminum hydroxide sensitized ; ④ high-dose group: 300μg Epimedium saponi + aluminum hydroxide sensitized. The lung inflammation and mucus secretion in mice were observed by HE staining. The total number of cells in bronchoalveolar lavage fluid and cell classification were detected. The levels of IL-4, IFN-γ and serum antigens in BALF and spleen homogenate were measured by enzyme-linked immunosorbent assay Specific Antibodies Validate Asthma Animal Models. Results With the increase of antigen concentration, pathological changes of lung showed obvious allergic inflammation. The total number of cells in bronchoalveolar lavage fluid of high dose group was (210.75 ± 78.80) × 106 / L and the number of macrophages was (48.65 ± 3.27)%, EOS number (24.37 ± 4.28)%, IL-4, serum antigen-specific IgE antibody, IgG1 antibody was significantly higher than the blank control group (P <0.05); bronchoalveolar lavage fluid, spleen The IFN-γ of the homogenate supernatant decreased compared with the blank control group (P <0.05). Conclusion The hay pollen successfully constructed mouse allergic airway inflammation animal model.