Effect Of Salidroside Via NLRP3 Signaling Pathway On Airway Inflammation In Asthma

Objective:To investigate the effect and mechanism of Salidroside(SAL)on airway inflammation in asthmatic mice,and to provide experimental basis for clinical application of SAL in the treatment of childhood asthma.Methods:Forty-five male BALB/c mice(18-22g weight)were selected at 6-8 weeks of age,The patients were randomly divided into 5 groups:normal control group,asthma model group,low concentration SAL group,high concentration SAL group and dexamethasone group.Except the normal group,all the other four groups used 200ul Phosphate Buffered Saline solution(Phosphate Buffered Saline,PBS)(10ug egg albumin OVA+2mg aluminium hydroxide adjuvant)given intraperitoneally to sensitize,Continuous inhalation with 2.5%OVA on the 21st day after sensitization for 7 days lasted 1/2 hours each time.Normal control group was treated by continuous inhalation with saline for 7 days on the 21st day.The typical symptoms of asthma such as scratching the nose and ears,wheezing and restlessness were observed in mice after stimulation,indicating that the model of asthma was successfully established.SAL(30mg/kg)and SAL(60mg/kg)were injected intraperitoneally in SAL group 1/2 hours before atomization.lmg/kg dexamethasone was injected intraperitoneally in the digia group,and 0.2ml saline was injected into the normal group.On the 29th day,the animals were anesthetized with alveolar lavage fluid(BALF).The right lung tissue was fixed by 4%formaldehyde solution,and the left lung was stored in-80℃,and then buried by paraffin.The contents of IL-18 and IL1βin BALF were detected by ELISA.Pulmonary tissue sections were stained with HE and pathological changes were observed under light microscope.Western blotting assay was used to detect the expression of NLRP3 and caspase-1 protein in lung tissue.Results:1.The levels of IL-18 and IL-1β in BALF of asthmatic model group were significantly higher than those in normal control group,The IL-18 and IL-1β contents in the high concentration SAL group were significantly lower than those in the model group(P<0.05),and there was a significant difference between the two groups(all P<0.05).2.Pathological changes of lung tissue:In normal group,all levels of bronchi structure were intact,and there was no infiltration of inflammatory cells around bronchi in the alveolar and pulmonary tissues.In asthma model group,the alveolar and tracheobronchial disorders,peritracheal edema,inflammatory cell infiltration,edema and inflammatory cell infiltration in SAL group were less than those in model group,and the pathological changes of lung tissues in mice group were similar to those in SAL group.3.Compared with normal group,the expression of NLRP3 and caspase-1 protein in lung tissue of asthmatic group increased significantly,Compared with the model group,the expression of NLRP3 and caspase-1 in SAL group decreased significantly(P<0.05).Conclusion:Salidroside can inhibit the airway inflammatory response in asthmatic mice,and its mechanism may be related to the inhibition of NLRP3 signaling pathway activation.