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作 者:刘珍[1] 刘金苹[2] 翟乃亮[1] 李淑翠[2] 范贤明[3]
机构地区:[1]滨州医学院临床学院,滨州市256603 [2]滨州医学院药理学教研室 [3]泸州医学院附属医院呼吸内科
出 处:《滨州医学院学报》2008年第3期177-178,197,共3页Journal of Binzhou Medical University
摘 要:目的观察地塞米松对博莱霉素(bleomycin,BLM)致肺纤维化1周大鼠肺泡巨噬细胞(AM)分泌TNF-α、IL-8和NO的影响,探讨地塞米松治疗特发性肺纤维化(IPF)的作用机制。方法取Wistar大鼠5只,向气管内灌注BLM复制肺纤维化模型后7 d处死动物,通过支气管肺泡灌洗获取AM,将其分为地塞米松(DEX)组和空白对照组,用DEX干预AM(空白对照组只加培养基),然后检测AM分泌TNF-α、IL-8、NO的能力。结果用地塞米松处理AM后的培养上清中,TNF-α、IL-8、NO含量减少,与空白对照组比较有显著性差异(P<0.05)。结论地塞米松可能通过减少AM分泌TNF-α、IL-8、NO,从而干预肺间质纤维化的发生发展。Objective To investigate the effect of dexamethasone on concentration of TNF-α, IL-8, NO produced by alveolar macrophages ( AMs )in bleomycin-induced rat pulmonary fibrosis. Methods Five adult female wistar rats were intratracheally instilled with BLM. After 7 days, the rats were killed by right ventricle of heart exsanguinations under ketamine anaesthesia and bronchoalveolar layage (BAL ) was performed to obtain AMs. AMs were divided into two groups, dexamethasone group and control group. Cultured medium was collected when cultured 36 hours after joining dexamethasone. The concentration of TNF-α, IL-8, NO in cultured medium was detected. Results The concentration of TNF-α, IL-8, NO in cultured medium coming from dexamethasone group was lower than that coming from control group. Condusion Dexamethasone could reduce the secretion of TNF-α, IL-8, NO in AMs ,which may be the possible mechanism of anti-fibrosis.
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