摘要
目的研究孟鲁司特(montelukast,MK)对哮喘豚鼠肺血管通透性和肺泡灌洗液(BALF)中一氧化氮(NO)水平的影响,探讨MK拮抗哮喘气道炎症的机制。方法制备卵白蛋白致敏豚鼠哮喘模型。通过豚鼠引喘潜伏期和跌倒率的变化评价MK对哮喘的拮抗作用;苏木精-伊红(HE)染色观察肺组织炎症的改变;伊文思蓝分光光度法测定哮喘豚鼠肺血管的通透性;硝酸还原酶法测定BALF中NO的含量。结果MK治疗组致敏豚鼠引喘潜伏期延长,跌倒率降低,肺组织炎症减轻;肺组织提取液中伊文思蓝含量及BALF中NO含量显著降低,与模型组相比差异有显著性。结论降低BALF中NO水平和肺毛细血管通透性,是MK拮抗哮喘气道炎症的重要机制。
Objective To study the effect of montelukast on pulmonary microvascular permeability and the level of NO in barbotage alveolar fluid(BALF) of asthmatic guinea pigs, and explore the possible mechanism of anti-airway inflammation of montelukast. Methods Experimental asthma model of guinea pigs was established by ovalbumin in vivo. The antagonistic effect of montelukast on asthmatic guinea pigs was evaluated by the changes of asthmatic latency and tumble ratio. The inflammation in the lungs of asthmatic guinea pigs was observered by HE staining. We used evans blue spectrophotometry for determination of pulmonary microvascular permeability. The content of nitric oxide (NO) in BALF was detected by the method of nitrore ductase. Results Montelukast prolonged the asthmatic latency and reduced tumble ratio of asthmatic guinea pigs. After treated with montelukast, the airway inflammation of asthmatic guinea pigs was relieved , and contents of evans blue in lung tissues and NO in BALF were lowered significantly. Conclusion Lowering the level of NO in BALF and pulmonary microvascular permeability is an important mechanism for montelukast to antagonize asthmatic airway inflammation.
出处
《江苏医药》
CAS
CSCD
北大核心
2005年第11期845-847,共3页
Jiangsu Medical Journal