氮卓斯汀对哮喘豚鼠炎症细胞粘附功能的影响

目的研究组胺H1 受体拮抗剂氮卓斯汀(Azelastine ,AZT)对哮喘豚鼠炎症细胞粘附功能的影响,探讨氮卓斯汀拮抗哮喘气道炎症的可能机制。方法以卵白蛋白致敏豚鼠制备哮喘模型。采用密度梯度离心法分离并计数支气管肺泡灌洗液(BALF)中嗜酸性粒细胞(EOS)和淋巴细胞(LC)的数量;采用ELISA法检测血浆和BALF中可溶性细胞间粘附分子 1(sICAM 1)和可溶性P选择素(sP S)的含量。通过荧光酶标记法在pharmaciaCAPSystem中测定血清和BALF中嗜酸性粒细胞阳离子蛋白(ECP)的水平。结果氮卓斯汀能显著降低哮喘豚鼠BALF中Eos和LC的数量;在氮卓斯汀治疗组,哮喘豚鼠血浆和BALF中sICAM 1和sP S的含量均显著降低,血清和BALF中ECP的含量也显著降低,与模型组相比均有显著性差异。结论氮卓斯汀能降低哮喘豚鼠sICAM 1、sP S和ECP的水平,抑制Eos和LC的粘附,减少其在气道的浸润。这可能是组胺H1 受体拮抗剂氮卓斯汀拮抗哮喘气道炎症的重要机制之一。

THE EFFECT OF AZELASTINE ON THE FUNCTION OF ADHESION OF INFLAMMATORY CELLS OF ASTHMATIC GUINEA PIGS

Objective To study the effect on the function of adhesion of inflammatory cells of asthmatic guinea pigs treated with azelastine, and explore the possible mechanism of azelastine for asthmatic airway inflammation. Methods Experimental asthma model of guinea pigs was induced by ovalbumin in vivo. The eosinophils and lymphocytes in BALF were separated by density gradient centrifugation. The content of sICAM-1 and sP-S in plasma and BALF was detected by enzyme-linkedimmunosorbent assay (ELISA). The level of ECP in serum and BALF was detected through fluorescence enzyme-labeled assay. Results The number of eosinophils and lymphocytes in BALF of asthmatic guinea pigs treated with azelastine decreased significantly. After the treatment with azelastine, the levels of sICAM-1 and sP-S in plasma and BALF lowered significantly. The levels of ECP in serum and BALF also decreased significantly. There were statistical differences between the therapeutic group and the model group. Conclusion Lowering the levels of sICAM-1, sP-S and ECP, inhibiting the function of adhesion and infiltration in airway of eosinophils and lymphocytes, may be an important mechanism for azelastine to antagonize asthmatic airway inflammation.