烟熏PM2．5颗粒建立COPD大鼠模型

Rat model of COPD established by inhalation with PM2.5

目的探讨高浓度PM2．5颗粒暴露建立COPD大鼠模型的可行性。方法40只Wistar大鼠随机分为正常对照组（A组）和PM2．5烟熏3个月组（B组），观察不同时期大鼠肺功能、BALF细胞计数及肺组织病理切片，并与A组进行比较。结果与A组相比，B组大鼠肺顺应性下降，气遭阻力增高；BALF中细胞总数增多，中性粒细胞数、中性粒细胞所占比例、淋巴细胞数、淋巴细胞所占比例也较A组增多，B组与A组之间的差异均有统计学意义；病理学观察显示，B组上皮细胞出现排列紊乱、部分增生、周围有平滑肌增生及炎细胞浸润，肺泡腔明显扩大、部分肺泡间隔出现断裂、肺泡相融合；B组肺泡破坏指数及平均内衬间隔均较A组明显增加。结论长期吸入高浓度PM2．5颗粒暴露可以成功建立大鼠肺气肿模型。

Objective To set a rat model of PM2.5-induced COPD. Methods Forty adult rats were randomly divided into two groups ： the control group and PM2.5-exposed group. Then contrast the data of lung function of rats, the counts of inflammatory cells were detected in BALF, and morphological manifestations. Results Compared with the control group, airway resistance of PM2.5-exposed group was higher,and dynamic lung compliance was lower, and there were more macrophages and neutrophils in BALF （all P 〈 0.05）. Morphological detection showed disruption of alveolar septa, significant enlarged airspace, and formation of emphysema, and part of the airway epithelial hyperplasia, inflammatory cell infiltration and proliferation of smooth muscle. Morphological quantitative analysis showed that model group average lining interval and alveolar damage index increased compared with normal control group. Conclusions PM2.5 can induce COPD stably in rat.