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机构地区:[1]深圳市人民医院麻醉科(暨南大学医学院附属第二医院),广东深圳518020
出 处:《国际医药卫生导报》2007年第16期57-59,共3页International Medicine and Health Guidance News
摘 要:目的探讨细胞表面粘附分子在呼吸爆发时PMN产生H2O2中的作用。方法用氧化酚红比色法来测定呼吸爆发时H2O2的产生量及CD11b、ICAM-1对此过程的影响。结果LPS激活PMNS后,其H2O2释放量明显增加,(15.3±3.50)μmol/L vs(3.81±0.41)μmol/L,P〈0.005。经CD11b单抗、ICAM-1单抗、CD11b+ICAM-1单抗预处理后,并没有影响H2O2的释放(P〉0.05)结论在本实验条件下,CD11b、ICAM-1的表达对LPS激活的PMNS释放H2O2不是必需的。Objective To investigate the role of the adhesion molecules in release of H2O2 by PMNs in the respiratory burst. Methods H2O2 realeasing in the respiratory burst and the effect of CDIIb, ICAM-1 were measured with a colorimetric method by spectrophotometer witch based on the principle of oxidation of phenol red . Results Activating PMNs with 100 ng/mlLPS resulted in the increasing of the apparent quantity of H2O2, (15.3±3.50) μmol/L vs (3. 81 ±0.41) μmol/L, P〈0.005).Anti-CD11bMoAb, anti-1CAM-1 MoAb and anti-CD11bMoAb +anti- ICAM-1MoAb did not affect the realeasing of H2O2(P〉0.05) Conclution The expression of CD11b and ICAM-1 is not involved in realease of H2O2 by PMNs in our experiments.
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