诱导型一氧化氮合酶在哮喘大鼠肺组织的表达

Expression of Inducible Nitric Oxide Synthase in Asthmatic Rat Lung

目的 观察哮喘大鼠肺组织中诱导型一氧化氮合酶 (i NOS)活性的表达 ,探讨一氧化氮在哮喘大鼠气道炎症中的作用。方法 用卵白蛋白作为致敏原制备哮喘大鼠模型 ,用 SP免疫组化染色方法检测肺组织 i NOS的表达并观察 i NOS在气道组织分布的改变。结果 哮喘大鼠肺组织 i NOS的表达阳性率 (90 % )明显高于正常对照组 (2 0 % ) (P<0 .0 0 1)。哮喘大鼠气道组织 i NOS表达阳性细胞主要位于气道上皮细胞、气道平滑肌细胞、血管内皮和平滑肌细胞、浸润的中性粒细胞和巨噬细胞 ,而淋巴细胞表达不明显。用甲基强的松龙处理后哮喘大鼠肺组织i NOS表达阳性率 (30 % )明显降低。结论 以上结果提示一氧化氮在哮喘气道炎症中起重要作用 ,用甲基强的松龙治疗哮喘可以使哮喘大鼠肺组织中 i NOS表达阳性率降低 。

Objective In order to study the role of nitric oxide (NO) during the airway inflammation of asthmatic rat, we investigated expression of inducible nitric oxide synthase (iNOS) in the lung tissue of asthmatic rats. Methods Animal model of asthmatic Wistar rats was developed by being sensitized and challenged with ovalbumin. Activities of iNOS were measured by using SP immunohistochemical method. Results In asthmatic rat group (n=10), lung tissue showed stronger immunostaining (90%) for iNOS than control group (20%) (P<0001). Immunostaining was mainly present in the bronchial epithelium, alveolar epithelium, bronchial smooth muscle, vascular endothelial and smooth muscle cells and inflammatory cells such as macrophages and neurophils. In glucocorticoid treated group (n=10), there was down regulation of iNOS immunoreactivity (30% positive) compared with control asthmatic rat group (20%). Conclusions The increased expression of iNOS in asthmatic rat lung tissue showed NO playing a critical role in asthmatic inflammation,otherwise expression of iNOS was inhibited by glucocorticoid.