动物造模 z-bio 2021-10-25 197

　　Objective: To understand the expression changes of dendritic cell surface factors OX62 and CD83 in the lungs of chronic obstructive pulmonary 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), chronic obstructive pulmonary model group (10 rats), CCL20 monoclonal antibody group (10 rats), and lipopolysaccharide was injected into the airway (2 times in total) ) Combined smoke stimulation (approximately 28 days) to induce COPD model. At the beginning of the experiment, rats in the monoclonal antibody group were injected intraperitoneally with CCL20 monoclonal antibody once. On the 29th day, the lung tissues of the rats were taken 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 lung tissue of rats in the model group was consistent with airway inflammation and emphysema. The pathological manifestations of the lungs of rats in the CCL20 monoclonal antibody group were significantly reduced compared with those in the COPD group. Compared with the healthy control group, the expression of OX62 in the lung tissue of rats in the COPD model group was significantly higher than that in the control group (P<0.05), while the expression of OX62 in the CCL20 monoclonal antibody group was lower than that in the COPD group (P <0.05). The expression of CD83 in the lung tissue of rats in the COPD model group was less than that in the control group (P <0.05), but="" there="" was="" no="" significant="" difference="" between="" the="" copd="" group="" and="" ccl20="" monoclonal="" antibody="" p="">0.05).

　　Conclusion: The incidence of COPD may be related to the increase in the expression of OX62 and the decrease in the expression of CD83 in the lungs. The use of CCL20 monoclonal antibody can partially inhibit this effect.