被动吸烟对致敏大鼠气道5-脂氧合酶及其mRNA表达的影响

Effect of passive smoking on the expressional levels of 5-lipoxygenase protein and mRNA in sensitized rats airway

目的通过研究吸烟对致敏大鼠气道5-脂氧合酶及其mRNA表达的影响，探讨吸烟对支气管哮喘（简称哮喘）气道炎症的影响，从而为临床上治疗吸烟哮喘提出实验依据。方法雄性Wistar大鼠30只，随机分为对照组、致敏组和吸烟致敏组，每组10只。后两组应用卵白蛋白致敏并长期（8周）吸入激发，制备哮喘模型；在激发第3周开始，将吸烟致敏组大鼠置于自制熏箱内进行被动吸烟。采用免疫组织化学及原位杂交法检测各组大鼠气道5-脂氧合酶蛋白及其mRNA的表达。结果①吸烟致敏组气道5-脂氧合酶蛋白的表达（32．58±2．78）明显高于致敏组（21．65±2．12）和对照组（15．38±1．68），差异有统计学意义（P值均〈0．01）；致敏组高于对照组，差异有统计学意义（P〈0．01）；②吸烟致敏组气道5-脂氧合酶mRNA的表达（34．68±2．90）高于致敏组（23．55±2．28）和对照组（15．78±1．72），差异有统计学意义（P值均〈0．01）；致敏组高于对照组，差异有统计学意义（P〈0．01）。结论吸烟可使致敏大鼠气道5脂氧合酶及其mRNA表达增多，加重气道炎症。

Objective To study the effect of smoking on airway inflammation of bronchial asthma （asthma） and put forward experimental basis for the treatment of asthma of smoking through researching the effect of smoking on the expressional levels of 5-lipoxygenase protein and mRNA in sensitized rats airway. Methods Thirty male Wistar rats were divided randomly into control group,sensitized group and smoking sensitized group. The rats of latter two groups were sensitized and challenged by ovalbumin to establish the asthmatic model. From the challenged third weeks, the smoking sensitized group rats were put in the self-made fumigating box to smoke passively. The expressions of 5-lipoxygenase protein and mRNA in airway were defected using immunohistochemistry and hybridization in situ in all rats of three groups. Results （1） The expression of airway 5-lipoxygenase protein （ 32.58 ± 2.78） were significantly higher than those of the sensitized group （ 21.65 ±2.12 ） and the control group （ 15.38 ± 1.68 ; all P 〈 0.01）, so did the sensitized group and the control group, （ P 〈 0.01）. （2）The expression of airway 5- lipoxygenase mRNA（34.68±2.90）were significantly higher than those of the sensitized group（23.55 ±2.28） and the control group（ 15.78±1.72;all P 〈0.01 ）, so did the sensitized group and the control group （ P 〈0.01）. Conclusions Smoking can increase the expession level of 5-lipoxygenase protein and mRNA in sensitized rats airway and aggravation airway inflammation.