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目的：探讨卡介苗对哮喘小鼠肺组织中PPAR-γ表达的影响及其意义。方法：30只健康雄性昆明种小鼠随机化原则分成正常对照组（A组）、哮喘模型组（B组）和卡介苗干预组（C组），每组10只。卵蛋白致敏法复制哮喘模型，B组小鼠于实验的第1、8、 15天分别给予卵蛋白与氢氧化铝混合腹腔注射。第22 天开始给予卵蛋白溶液以压缩雾化器为动力雾化吸入激发哮喘，每日一次，每次30min。连续激发7天；C组小鼠每周一次皮内注射0.025mg BCG，连续3次，距首次皮内注射4周后按B组方法致敏和激发；A 组予以等量生理盐水代替致敏液及雾化液进行腹腔注射与雾化吸入。检测细支气管炎症细胞浸润及肺组织病理， RT-PCR和western blotting方法检测肺组织PPAR-γ的表达情况。结果：哮喘组出现了明显气道炎症细胞浸润，上皮脱落、炎性细胞渗出、结构紊乱、PPAR-γ表达下降。卡介苗干预组炎症细胞数下降，炎症反应减轻，PPAR-γ 表达明显增加，差异具有统计学意义（P<0.01）。结论：卡介苗可通过上调表达PPAR-γ，减少炎症细胞的浸润，抑制炎症反应，从而可能防止气道重塑，该研究为卡介苗提供新的临床应用领域。

英文摘要:

Objective: To investigate the effect of bacillus Calmette-Guerin (BCG) on the expression of peroxisome proliferator- activated receptor-γ (PPAR-γ) in the lung tissue of asthmatic mice and its significance. Methods: Thirty adult male Kunming mice were randomly divided into three groups (n=10): the control group (group A), asthmatic group (group B), BCG group (group C). The asthmatic model was established by the ovalbumin challenge method. Mice in group B were given ovalbumin and aluminum hydroxide mixture by intraperitoneal injection at 1, 8, 15 day. Mice were inhaled ovalbumin solution drived by compressed Atomizer for asthma once a day (every 30min) from 22 day and continuously challenged for 7 days. Mice in group C were weekly given 0.025mg BCG by intradermal injection and continuously injected for 3 times. After 4 weeks, mice were sensitized and challenged by the method as group B. Mice in group A were given normal saline solution. The bronchiole inflammatory cell infiltration, remodeling index and lung tissue histopathological were observed. Expressions of PPAR-γ in lung tissue were assayed by RT-PCR and western blotting. Results: There were obviously bronchiole remodeling response and inflammatory cell infiltration in group B, which can be inhibited by BCG. RT-PCR and western blotting showed that the expression of PPAR-γ in lung tissue was down-regulated in group B compared to that of group A (P<0.05). While the expression of PPAR-γin lung tissue was increased in group C after BCG treatment. Conclusion: BCG reduced infiltration of inflammatory cells and inhibited the inflammatory response to prevent airway remodeling by up-regulating the expression of PPAR-γ. The study provides a new clinical application for BCG.

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