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作 者:汪铮[1] 张劲农[1,2] 胡小飞[1] 彭梅君[1] 王小溶[1] 赵婷婷[1] 向敏[1,2] 付薇[1,2]
机构地区:[1]武汉协和医院呼吸病研究所,湖北武汉430022 [2]武汉协和医院呼吸内科
出 处:《医学信息(医药版)》2009年第8期1-3,共3页
摘 要:【摘要】目的:探讨己酮可可碱(PTX)对香烟提取物激活原代培养大鼠肺泡巨噬细胞IP-10表达的作用。方法:肺泡灌洗法收集Wistar大鼠肺泡巨噬细胞,贴壁纯化培养,制备香烟烟雾提取物(CSE),分别以1mol/L、10mol/L、100mol/L和1000mol/LPTX加入含5%CSE的培养体系中,干预24小时后ELISA法检测上清中IP-10含量。RT—PCR.法检测细胞IP-10mRNA表达。结果:1、10、100和1000mol/LPTX干预后,培养上清中IP-10的含量分别为15.82±0.43pg/ml、12.41±0.36pg/ml、7.92±0.67pg/ml、5.13±O.31pg/ml,IP-10mR.NA的表达强度分别为0.241±0.056、0.432±0.034、0.854±0.094、0.772±0.055。结论:PTX干预能剂量依赖性地抑制香烟烟雾诱导的大鼠肺泡巨噬细胞IP-10表达,该作用可能是PTX拮抗肺内炎症激活和抑制慢性吸烟肺气肿形成的机制之-。Objective To investigate the effect of pentoxifylline (PTX) on cigarette smoke extract (CSE)-induced IP-10 production in rat alveolar macrophages. Methods PTX of different concentrations and CSE were added into rat alveolar macrophage primary cultures (5% VN each). 24 hours later, the culture samples were collected for determination of IP- 10 concentration and IP-10 mRNA expression level. Results The level of IP-10 was 15.82± 0.43 pg/ml, 12.41±0.36 pg/ml, 7.92± 0.67 pg/ml and 5.13 ± 0.31 pg/ml, and the relative densometry of IP- 10 mRNA was 0.241 ± 0.056, 0.432±0.034, 0.854±0.094, 0.772± 0.055 after CSE and PTX exposure, respectively. Conclusion PTX inhibits CSE-induced IP-10 expression in a dose-dependent manner, which may serve as one of the mechanisms involved in its preventive effect on CSE-induced lung inflammation.
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