Objective To investigate the effects of dexamethasone on expressions of epithelial neutrophil activating protein-78 (ENA-78) and transforming growth factor- beta 1 (TGF-β1) in neutrophil of asthma rats.Methods Thirty male SD rats were randomly divided into three groups on average, including asthma group, control group and dexamethasone treated group. In this experiment, the rat model of asthma were established by sentization and challenge with ovalbumin. Blood neutrophil were isolated and purified. The expression of ENA-78 was detected by flow cytometry. The expression of TGF-β1 was detected by immunohistochemical method in blood neutrophil and bronchial wall. Results Expression of ENA-78 in blood neutrophil in dexamethasone treated group(71.82 ±8. 87 mean fluorescence intensity)was lower than that in asthma group, but higher than that in control group(all P ＜0. 01). And expressions of TGF-β1 protein in dexamethasone treated group(0. 173 ± 0. 014,0. 202 ± 0. 019 optical density, respectively) was lower than that in asthma group(all P ＜0. 01) ,but higher than that in control group(all P ＜0. 01). There were significant positive correlation between ENA-78 expression at blood neutrophil and numbers of total inflammation cells in bronchoalveolar lavage fluid (n = 29, γ = 0. 762, P ＜ 0. 01). Conclusion The beneficial effect of glucocorticoid(dexamethasone) on airway inflammation in asthma rats could be at least in part due to their direct inhibitory effect on ENA-78 and TGF-β1 protein generation by neutrophil.

AIM: To observe the changes of polymorphonuclear leukocytes (PMN), neutrophil elastase (NE) and myeloperoxidase (MPO) expression in rat asthma. METHODS: Eighteen rats were randomly divided into two groups on average, including asthma group and control group. The rat model of asthma was established by the ovalbumin (OVA) challenge methods. Blood PMN were isolated and purified. The protein expression of MPO were detected by immunohistochemistry and chromatometry techniques. NE was detected by ELISA. RESULTS: (1) Immunohistochemistry showed that the levels of MPO expression around bronchus and in purified PMN in asthma group were significantly increased compared with those in control group (P

OBJECTIVES: Cardiac hypertrophy and fibrosis are major pathological manifestations observed in left ventricular remodeling induced by angiotensin II (AngII). Low-intensity pulsed ultrasound (LIPUS) has been reported to ameliorate cardiac dysfunction and myocardial fibrosis in myocardial infarction (MI) through mechano-transduction and its downstream pathways. In this study, we aimed to investigate whether LIPUS could exert a protective effect by ameliorating AngII-induced cardiac hypertrophy and fibrosis and if so, to further elucidate the underlying molecular mechanisms. METHODS: We used AngII to mimic animal and cell culture models of cardiac hypertrophy and fibrosis. LIPUS irradiation was applied in vivo for 20 min every 2 d from one week before mini-pump implantation to four weeks after mini-pump implantation, and in vitro for 20 min on each of two occasions 6 h apart. Cardiac hypertrophy and fibrosis levels were then evaluated by echocardiographic, histopathological, and molecular biological methods. RESULTS: Our results showed that LIPUS could ameliorate left ventricular remodeling in vivo and cardiac fibrosis in vitro by reducing AngII-induced release of inflammatory cytokines, but the protective effects on cardiac hypertrophy were limited in vitro. Given that LIPUS increased the expression of caveolin-1 in response to mechanical stimulation, we inhibited caveolin-1 activity with pyrazolopyrimidine 2 (pp2) in vivo and in vitro. LIPUS-induced downregulation of inflammation was reversed and the anti-fibrotic effects of LIPUS were absent. CONCLUSIONS These results indicated that LIPUS could ameliorate AngII-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway, providing new insights for the development of novel therapeutic apparatus in clinical practice.