Yeadon M, Price R
Department of Pharmacology, Wellcome Foundation Ltd., Beckenham, Kent.
Br J Pharmacol. 1995 Nov;116(6):2545-6. doi: 10.1111/j.1476-5381.1995.tb17204.x.
There is some evidence that nitric oxide synthase (NOS) is induced in the lungs of patients with allergic asthma, but the mechanism of this is not understood. The aim of the present study was to investigate whether the levels of NOS in rat lung could be altered by exposure of the animals to aerosols of allergen (ovalbumin). Brown-Norway rats were actively sensitized to ovalbumin, raising a mixed IgE/IgG antibody response. The levels of total and calcium-independent NOS in lung tissue homogenates were elevated at 6 h and 24 h after allergen exposure in sensitized rats but not in unsensitized rats. The induction was not due to contaminating lipopolysaccharide in the challenge solution. The allergen-induced increase in calcium-independent lung NOS was inhibited by pretreatment of the animals with the corticosteroid betamethasone (3 mg kg-1 i.p., 1 h prior to and 6 h after allergen). These results show that allergen challenge induces calcium-independent NOS in the lungs of sensitized rats, a process inhibited by an anti-inflammatory corticosteroid.
有证据表明,过敏性哮喘患者的肺部会诱导产生一氧化氮合酶(NOS),但其机制尚不清楚。本研究的目的是调查将动物暴露于过敏原(卵清蛋白)气雾剂中是否会改变大鼠肺中NOS的水平。将棕色挪威大鼠主动致敏于卵清蛋白,引发混合的IgE/IgG抗体反应。致敏大鼠在接触过敏原后6小时和24小时,肺组织匀浆中总NOS和钙非依赖性NOS的水平升高,而未致敏大鼠则未升高。这种诱导不是由于激发溶液中污染的脂多糖所致。用皮质类固醇倍他米松(3mg kg-1腹腔注射,在接触过敏原前1小时和后6小时)预处理动物,可抑制过敏原诱导的钙非依赖性肺NOS增加。这些结果表明,过敏原激发可在致敏大鼠的肺部诱导产生钙非依赖性NOS,这一过程可被抗炎皮质类固醇抑制。