Promoting Effect of Naringin on Airway Inflammatory Cell Apoptosis in Asthmatic Mice and Its Mechanism
Objective To investigate the regulation of naringin on apoptosis of airway inflammatory cells in asthmatic mice and its relationship with Tas2rs.Methods 36 BALB/c mice were randomly divided into 6 groups(n=6):blank control group,ovalbumin model group(OVA),dexamethasone group(10 mg·kg-1,positive control drug),naringin low,medium and high dose groups(10,20,40 mg·kg-1).Airway asthma was induced by OVA in all groups except the blank control group.After continuous administration of solvent,dexamethasone or naringin for 6 days,the respiratory function and the number of cells in alveolar lavage fluid of mice were measured,the lung and airway morphology of mice were observed,respiratory resistance(Rrs),lung elastic resistance(Ers)and respiratory compliance(Crs)were measured,and mRNA expression levels of lung tissue-related pro-apoptotic factors were measured.The mRNA expression levels of Tas2rs and its downstream genes were determined.Results Compared with OVA model group,naringin could dose-dependent decrease Rrs and Ers,increase Crs,and decrease the number of leukocytes,eosinophils,lymphocytes and neutrophils.Compared with OVA model group,the infiltration of inflammatory cells in lung tissue was significantly reduced in high-dose naringin group,and the mRNA expression levels of Tas2r108,Tas2r135,Tas2r143 and their downstream target genes α-gust and Trpm5 in lung and airway tissue were significantly decreased.The mRNA expression levels of proapoptotic factors P53,Bax and Casp3 were increased,while the mRNA expression levels of apoptosis inhibitor Bcl2 were decreased.Conclusion Naringin prophylactic administration can promote the activation of airway Tas2rs signal,decrease the number of airway inflammatory cells and alleviate airway injury in asthmatic mice.Naringin as a Tas2rs agonist can be developed as a potential anti-asthmatic agent.
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