The Modulation Of Heat Shock Protein70on The Expresson Of Syntaxinl In Asthmatic Model

Purpose To investigate the relationship between heat shock protein70(HSP70) andsyntaxin1(SYX1) in bronchopulmary tissues in asthmatic rat model and its clinicalsignificances; to observe the expression of HSP70and SYX1in asthmatic rat modeltreated with DXM.Methods Thirty adult Wister rats were randomly divided into three groups: controlgroup (n=10), asthma group (n=10) and a group of asthma treated with dexamethasone(Asthma+DXM group, n=10). Asthma rat model was established by sensitization andstimulation with ovalbumin (OVA) conjuncted with Al (OH)3。The rats of DXM groupwere treated with an intraperitoneal injection of DXM30minutes before OVA challenge.The control group received an intraperitoneal injection of1.5ml saline and inhale salineaerosol without OVA. The model was confirme by the observation of symptoms of therats after sensitization and stimulataion with OVA, and the pathological histologicsection of Hematoxylin and Eosin (HE) stain of bronchopulmonary tissue.Immunohistochemistry, western bloting and RT-PCR were used to evaluate the proteinand gene expression of HSP70and SYX1in bronchopulmonary tissues of these groups.Co-immunoprecipitation (CO-IP) assay was used to identify the interaction betweenHSP70and syntaxin1.Results The asthmatic rat model was established successfully. The asthmatic rats hadthe symptoms of restlessness, breathlessness, abdominal respiratory ryhythms and wheezing rale after stimulating with OVA. These symptoms were not observed incontrol group and were much milder in asthma+DXM group than that in asthmaticgroup. Examination of lung tissue specimens from asthmatic group demonstratedcellular peribronchial and perivascular infiltrates consisting of inflammatory cells, suchas neutrophils, lymphocytes, and eosinophils. In addition, there was hyperplasia of themucus-secreting goblet cells lining the bronchial epithelium. In contrast, DXMtreatment produced a marked decrease in both cellular infiltrates and inflammatorychanges within the bronchial mucosa. Only a small amount number of inflammatorycell infiltration around the airways was found in control group. Compared to the controlgroup, the expression of HSP70and SYX1in protein and gene levels both increasedsignificantly in asthma group (P<0.05，P<0.05). The expression of HSP70and syntaxin1in asthmatic rats treated with DXM was significantly reduced when compared withasthma group (P<0.05，P<0.05). However, there was no significant difference betweenasthmatic rats treated with DXM and control group (P>0.05, P P>0.05). Hsp70was seenin the cytoplasm of airway epithelial cells, while syntaxin1near the apical cell surfaceof the airway epithelial cells. CO-IP indicated that HSP70has a property to interact withsyntaxin1.Conlusion The upregulation of HSP70and SYX1was detected in asthmaticbronchopulmonary tissues and there is a modulation of HSP70on presynaptic protein,SYX1, which may be involved in the pathogenesis of asthma, and their expressionlevels was negative regulated by dexamethasone.