Study The Effects Of Salidroside On Apoptosisof Pulmonary Vascular Endothelial Cells In Rats With Chronic Airway Inflammation

Objective:Establish a rat model of chronic airway inflammation and intervene with salidroside,to investigate the mechanism of salidroside in regulating chronic airway inflammation and pulmonary vascular endothelial apoptosis in rats.Methods:Using group control studies,according to random number table method,all of 60 SD rats were randomly divided into normal control group,chronic airway inflammation model group and salidroside intervention group,20 rats in each group.Through exposing rats to a combination of cigarette smoke and lipopolysaccharide to prepare model of chronic airway inflammation.The rats in the normal group were intraperitoneally injected with 0.2 ml of normal saline per day.The rats in the model group were smoked daily,plusinjecting 0.2 ml of 200 ug LPS into the trachea at d1 and d15 days.The rats in the intervention group were injected intraperitoneally 40 mg/kg salidrosideon the basis of the model group.4 weeks laterrat lung tissue samples were taken,HE staining was used to observe the degree of airway inflammation in lung tissue.The expression of NF-κB P65,Bax,Bcl-2 and Cleaved caspase3 in lung tissue cells was detected by Western blot,Apoptosis index of pulmonary vascular endothelial cells was measured by TUNEL.Results:1.Compared with the normal control group,the alveolus in the terminal lung tissueof the model group were enlarged,the alveolar wall became thinner,the vascular bed of the alveoluswas sparse,and the thinned alveolar wall ruptured to form a pulmonary bullae.NF-κB p65、Cleaved caspase-3 in lung tissue and the ratio of Bax/Bcl-2increased significantly(P<0.01),and the apoptosis of pulmonary vascular endothelial cells around alveolus was significant(P<0.01).2.Compared with the normal control group,the alveolus in the terminal lung tissueof the intervention group was slightly enlarged,there was a uniform capillary bed around the alveoli,there was no obvious rupture and fusion of the alveoli,no macrobubble formation,NF-κB p65、Cleaved caspase-3 in lung tissue and the ratio of Bax/Bcl-2 increased slightly(P<0.05),and the apoptosis of pulmonary vascular endothelial cells around the alveoli was slightly increased(P<0.05).3.Compared with the model group,the alveolus in the terminal lung tissue of the intervention group had a reduced degree of alveolar enlargement,and there was still a uniform capillary bed around the alveolar wall.No obvious alveolar wall rupture and pulmonary bullae were observed.NF-κB p65、Cleaved caspase-3 in lung tissue and the ratio of Bax/Bcl-2 decreased significantly(P<0.01),and the degree of apoptosis of pulmonary vascular endothelial cells around alveolar cells was lighter(P<0.01).Conclusions:1.Salidroside has a certain inhibitory effect on chronic airway inflammation and alveolar capillary endothelial apoptosis.2.Salidroside may inhibit chronic airway inflammation through NF-κB/Bcl-2 pathway,and salidroside inhibits chronic airway inflammation.3.Salidroside may provide new ideas for the prevention and treatment of chronic airway inflammation.