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作 者:夏锦芳[1] 王砚[1] 唐法娣[1] 徐巧萍[1] 赵小京[1] 刘君波[1] 朱有法[1]
机构地区:[1]浙江大学医学院呼吸药物研究实验室,杭州310058
出 处:《中国药学杂志》2010年第6期423-428,共6页Chinese Pharmaceutical Journal
基 金:浙江省科技计划项目(2008c23066)
摘 要: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 investigate the effect of spearmint oil on airway inflammation and the expression of interleukin-8 ( IL- 8 ) and CC-ehemokines receptors 2 (CCR2) in rats with chronic obstructive pulmonary disease (COPD). METHODS COPD model was induced by intratracheal instillation of lipopolysaccharide(LPS) and passive smoking for 12 weeks in rats, and COPD rats were treated with spearmint oil for 4 weeks. After COPD was induced,the methaeholine (Mch)-induced airway resistance (RL) and total and differential cell count in bronchoalveolar lavage fluid(BALF) were measured . The pathologic changes of long tissue were observed by HE, AB-PAS and Masson staining , and IL-8 content and CCR2 expression were measured. The effect of spearmint oil was deter- mined. RESULTS Spearmint oil 30,100 and 300 mg · kg^-1 significantly reduced leucocyte, neutrophile , lymphocyte and macro- phage numbers in BALF, and attenuated bronchiolitis, pulmonary interstitial inflammation and inflammation cell infihration, and decreased the destruction of puhnonary alveolus and the thickness of bronchioles walls, and inhibited goblet cell proliferation. Spearmint oil 100 and 300 mg · kg^-1 significantly reduced IL-8 in lung homogenate and spearmint oil 30,100 and 300 mg · kg^-1 significantly decreased the expression of CCR2 in lung tissues. CONCLUSION Spearmint oil has protective effect on lung injury in COPD rats ,since it improves pulmonary inflammation, goblet cell proliferation , collagen deposition, emphysema, airway remodeling. The mechanism may include reducing IL-8 content and decreasing CCR2 expression in lung tissue.
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