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目的观察留兰香油对慢性阻塞性肺疾病(COPD)大鼠气道炎症反应与白细胞介素(IL)-8和CC-亚族超化因子受体2(CCR2)受体表达的影响。方法用反复被动吸烟和气道内滴入脂多糖12周建立大鼠COPD模型后,留兰香油灌胃治疗4周。测定气道阻力,计数大鼠COPD模型支气管肺泡灌洗液(BALF)中白细胞总数及分类,肺组织病理切片HE、AB-PAS和Masson染色观察气道炎症并行半定量评分及病理图像的形态学测量分析,测定IL-8含量和CCR2的表达水平。结果留兰香油30、100和300mg.kg-1能明显降低BALF中白细胞总数、分类中中性粒细胞、淋巴细胞及单核巨噬细胞;减轻细支气管炎和肺间质炎及炎症细胞浸润;能明显减少肺泡破坏,使细支气管壁变薄以及抑制杯状细胞增生,能使气道壁胶原沉积厚度明显降低。留兰香油100和300mg.kg-1能明显降低肺组织匀浆中的IL-8含量,留兰香油30、100和300mg.kg-1能明显降低肺组织CCR2表达水平。结论留兰香油对熏烟和脂多糖引起的大鼠COPD模型的肺部炎症、肺气肿、杯状细胞增生、胶原沉积增厚、气道重塑有改善作用,其机制可能是留兰香油降低了肺组织IL-8的含量和CCR2受体的表达。
Objective To observe the effects of Spearmint oil on the airway inflammatory reaction and the expression of interleukin (IL) -8 and CC-subunit 2 (CCR2) receptors in chronic obstructive pulmonary disease (COPD) rats. Methods After repeated passive smoking and intratracheal instillation of lipopolysaccharide for 12 weeks, rats were treated with spearmint oil for 4 weeks. The airway resistance was measured. The total number and classification of leukocytes in the bronchoalveolar lavage fluid (BALF) of the COPD model rats were counted. The lung tissues were stained with HE, AB-PAS and Masson to observe the semi-quantitative airway inflammation and histomorphology Measurement and analysis, determination of IL-8 content and CCR2 expression levels. Results Spearmint oil 30,100 and 300mg.kg-1 can significantly reduce the total number of white blood cells in BALF, classification of neutrophils, lymphocytes and mononuclear macrophages; reduce bronchiolitis and interstitial lung inflammation and inflammatory cell infiltration ; Can significantly reduce alveolar damage, thinning the bronchial wall and inhibit goblet cell proliferation, can make the airway wall collagen deposition thickness was significantly reduced. Spearmint oil 100 and 300mg.kg-1 can significantly reduce the content of IL-8 in lung tissue homogenate. Spearmint oil 30,100 and 300mg.kg-1 can significantly reduce the expression of CCR2 in lung tissue. Conclusion Spearmint oil can improve lung inflammation, emphysema, goblet cell proliferation, thickening of collagen deposition and airway remodeling in COPD model rats induced by fumigation and lipopolysaccharide. The mechanism may be spearmint oil Reduced lung tissue IL-8 content and CCR2 receptor expression.