椒目油对哮喘大鼠肺组织Fas/FasL表达水平和肺血管通透性的影响

Effects of Zanthoxylum Seed Oil on Pulmonary Microvascular Permeability and Expression of Fas/FasL in Lung Tissue of Asthmatic Model in Rats

目的:观察椒目油(zanthoxylum seed oil,ZSO)对支气管哮喘大鼠肺组织Fas/FasL表达水平和肺血管通透性的影响,为临床应用椒目油治疗哮喘提供实验证据和理论支持。方法:将雄性SD大鼠80只随机分为正常对照组、哮喘模型组、地塞米松治疗组和椒目油治疗组,每组各20只。以卵白蛋白(ovalbumin,OVA)腹腔注射致敏和雾化吸入激发建立哮喘大鼠模型,以免疫组化ABC法检测肺组织中Fas/FasL蛋白的表达,伊文思蓝(evans blue dye,EBD)分光光度法检测肺血管通透性。结果:椒目油和地塞米松均能增强哮喘大鼠肺组织淋巴细胞表面Fas/FasL的蛋白表达;与哮喘模型组相比较,有统计学意义(P<0.05)。哮喘模型组大鼠肺内EBD浓度显著高于对照组(P<0.01),而与哮喘组相比,椒目油和地塞米松均能显著缓解EBD的升高(P<0.01)。结论:椒目油可有效降低哮喘大鼠肺血管通透性,可能通过增强Fas/FasL蛋白表达而促进炎症局部淋巴细胞凋亡减轻哮喘气道炎症反应。

Objective： To study the effects of zanthoxylum seed oil （ZSO） on pulmonary microvascular permeability and Fas/FasL in lung tissue of asthmatic model in rats and to provide theoretical basis for treatment of bronchial asthma using zanthoxylum seed oil. Methods： Eighty SD rats were divided into four groups： normal control group, asthmatic model group, dexamethasone treatment group and zanthoxylum seed oil treatment group, 20 rats in each group. Asthmatic models of rats were constructed by immunization of in- traperitoneal injection with saline ovalbumin（OVA）and challenged by inspiration with nebulized OVA. Protein expression of Fas/FasL in lung tissues were assayed by immune histochemistry. The levels of pulmonary microvascular permeability were determined using evans blue dye （EBD）spectrophotometry. Results： Protein expression of Fas/FasL in lung tissue in dexamethasone group and zanthoxylum seed oil group were potentialized, and were superior to those in normal control group （P〈0.05）. In the asthmatic model group, the contents of EBD in lung tissues were significantly higher than those in normal control group （P〈0.01）..The contents of EBD of both zanthoxylum seed oil and dexamethasone group were significantly lower than those of asthmatic model group （P〈0.01）. Conclusions： Zanthoxylum seed oil can decrease the level of pulmonary microvascular permeability and promote apoptosis of local lymphocyte by increasing gene expression of Fas/FasL to antagonize asthmatic airway inflammation.