动物造模 z-bio 2022-06-06 867

　　Objective: To understand the expression changes of dendritic cell surface factors OX62 and CD83 in the lungs of COPD rats, and to explore the intervention effect of CCL20 antibody.

　　Methods: Thirty healthy Wistar rats were selected and randomly divided into healthy control group (10 rats), COPD model group (10 rats) and CCL20 monoclonal antibody group (10 rats). ) combined with smoke stimulation (about 28 days) to induce COPD model. At the beginning of the experiment, the rats in the monoclonal antibody group were intraperitoneally injected with CCL20 monoclonal antibody once. On the 29th day, the lung tissue of the rats was collected to observe the pathological changes, and the expression changes of the surface factors OX62 and CD83 of the lung dendritic cells (DC) were detected by immunohistochemistry.

　　RESULTS: The HE staining of the lung tissue of the rats in the model group was consistent with the manifestations of airway inflammation and emphysema, and the pathological manifestations of the lungs in the CCL20 monoclonal antibody group were significantly less than those in the COPD group. Compared with the healthy control group, the expression of OX62 in the lung tissue of the COPD model group was significantly higher than that of the control group (P < 0.05), while that in the CCL20 mAb group was lower than that in the COPD group (P < 0.05). The expression of CD83 in the lung tissue of the COPD model group was less than that of the control group (P < 0.05), but there was no significant difference between the COPD group and the CCL20 mAb group (P > 0.05).

　　Conclusion: The pathogenesis of COPD may be related to the increased expression of OX62 and the decreased expression of CD83 in the lungs, and the use of CCL20 mAb can partially inhibit this effect.