Lehmann B, Kämpf A, Scheuch D W
Medizinische Akademie Carl Gustav Carus Dresden Institut für Pathologische Biochemie, DDR.
Biomed Biochim Acta. 1990;49(5):375-83.
Alveolar macrophages of normal and endotoxin--treated rats were stimulated in suspension by calcium ionophore A 23187. After solid phase extraction and isocratic separation by HPLC the lipoxygenase products (Leukotriene B4, 5-hydroxyeicosatetraenoic acid and 12-hydroxyeicosatetraenioc acid) were quantified. Unlike alveolar macrophages of control animals, alveolar macrophages of endotoxin treated rats showed an increased synthesis of lipoxygenase products (Leukotriene B4: 1.6fold; 5-hydroxyeicosatetraenoic acid: 2.1fold; 12-hydroxyeicosatetraenoic acid: 1.3fold). Our results suggest that in vivo endotoxin disturbs the mechanisms of arachidonic acid liberation in alveolar macrophages.
用钙离子载体A 23187对正常大鼠和经内毒素处理的大鼠的肺泡巨噬细胞进行悬浮刺激。经固相萃取和高效液相色谱等度分离后，对脂氧合酶产物（白三烯B4、5-羟基二十碳四烯酸和12-羟基二十碳四烯酸）进行定量。与对照动物的肺泡巨噬细胞不同，经内毒素处理的大鼠的肺泡巨噬细胞显示脂氧合酶产物的合成增加（白三烯B4：1.6倍；5-羟基二十碳四烯酸：2.1倍；12-羟基二十碳四烯酸：1.3倍）。我们的结果表明，体内内毒素会干扰肺泡巨噬细胞中花生四烯酸释放的机制。
