目的: 探究慢性阻塞性肺疾病(chronic obstructive pulmonary disease, COPD)大鼠肠黏膜相关炎症因子的调控机制。方法: 将20只雄性wister大鼠随机分为空白对照组、COPD模型组,每组10 只。通过烟熏联合气道内滴注脂多糖(lipopolysaccharide, LPS)法建立COPD大鼠模型。确认造模成功后,取各组大鼠结肠黏膜组织,透射电镜下观察结肠黏膜形态学变化;ELISA测定大鼠结肠黏膜匀浆TNF-α、IL-1β、MUC2的含量。结果: (1)与空白组比较,模型组大鼠存在结肠黏膜微观结构损伤,包括杯状细胞数目减少(P＜0.001)、绒毛长度降低(P＜0.001)、隐窝深度降低(P＜0.001);(2)与空白组比较,模型组大鼠存在炎症因子增多,ELISA结果显示TNF-α、IL-1β表达均增加(P＜0.001),MUC2表达减少(P＜0.001)。结论: COPD大鼠存在结肠黏膜微观结构及化学屏障损伤,COPD大鼠结肠黏膜内存在慢性炎症因子浸润。
Objective: To explore the regulation mechanism of intestinal mucosal inflammatory factors in rats with chronic obstructive pulmonary disease (COPD). Methods: Twenty male Wister rats were randomly divided into blank control group and COPD model group, with 10 rats in each group. The COPD rat model was established by smoking combined with intratracheal instillation of lipopolysaccharide (LPS). After successful modeling, the colonic mucosa of rats in each group was taken and the morphological changes of colonic mucosa were observed under transmission electron microscope. The contents of TNF-α, IL-1β and MUC2 in colonic mucosa homogenate of rats were determined by ELISA. Results: (1) Compared with the blank group, the rats in the model group had colonic mucosal microstructure damage, the number of goblet cells was decreased (P＜0.001), the length of villi was decreased (P＜0.001), and the depth of crypt was decreased (P＜0.001). (2) Compared with the blank group, there were more inflammatory factors in the model group, and the results of ELISA showed that the expressions of TNF-α and IL-1β were increased (P＜0.001), the expression of MUC2 was decreased (P＜0.001). Conclusion: COPD rats have colonic mucosal microstructure and chemical barrier damage, and there is chronic inflammatory factor infiltration in the colonic mucosa of COPD rats.
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