| Bronchial asthma is a chronic airway disease characterized by chronic inflammation and airway remodeling. Remodeling is the consequence of repeated damage and repair of airway by chronic inflammation, which may contribute to bronchial narrowing and airway hypersensitivity. Studies have shown that expressional disorder of many inflammational gene and abnormal regulation of multipal cell proliferation and apoptosis, including eosinophils, lymphocytes, mast cell, epithelial cell, smooth muscle cell and fibroblast, may be involved in the inflammation and construction change in airway. Peroxisome proliferator-activated receptor-gama (PPAR Y ) , a member of nuclear receptor surperfamily, known as regulating the differentiation and metabolism of adipocyte at first, recently is demonstrated to be related to inflammation and cell turnover. PPAR Y may expressed in the cells of lung and contribute to airway inflammation and remodeling.There are few article about regulation of peroxisome proliferator-activated receptor gama expression in human asthmatic airways and relationships with proliferation, apoptosis, and airway remodeling.Objective In the present study, we developed the asthmatic SD rat models for investigating airway remodeling. Immunohistochemical technique was used to estimatethe expression of PPAR y , PCNA and Caspase-3 in airway wall and cells in around . We try to explore the relationships among the expression of PPAR Y ,cell proliferation and apoptosis. Dexamethasone was administered as a therapeutic drug to study its function in regulating the expression of PPAR V and reversing the informed airway remodeling.Materials and Methods 39 healthy male SD rats weighting 130-170g wererandomly divided into three groups: (A) normal group, (B) model group, (C) dexamethasone group, each group contains 13 rats. Rats of group B and C were actively sensitized on 1st day and 14th day with 1ml intraperitoneal injections of solution containing lOOmg of ovalbumin and lOOmg aluminium hydroxide used as adjuvant , rats of group A were injected 1ml saline solution. Challenges for group B and C were performed every other day by inhaling 1% ovalbumin from the 16th day, while saline solution was for group A as subtitute. Each exposure lasting 20 min and challenges were 15 times in total. From the 46th day, 25% dexamethasone was inhaled 20min for group C every other day before challenges, there are 30min interval between two treatments; while saline solution for group A and B as consoling treatment. All rats were killed on 65th day by intraperitoneal injections of Phenobarbital. The tissue of lung must be syringed through right ventricle and fixed by 4% polyformaldehyde in vitro and in vivo before making frozen sections. General histologic characteristics and the collagen deposition degree were observed through stained sections using haematoxylin -eosin stain method and picrosirius red technique. The expression of PPAR Y , PCNA and Caspase-3 was observed from the immunohistochemical stained slides. Employing computer-asisted image analysis, each selected section was quantified under a 10 X objective microscope to measure the depth of airway epithium, smooth muscle, submucosa and the area of collagen deposition; count the staining positive cell in airway wall and surrouding. The statistical data were expressed by mean SD, one-way ANOVA and T test was used to compare the means of multiple variables.Results (1) There was no difference between group B and C beforetreatment(P>0.05) , inhaling dexamethasone can obviously decrease the severity of asthma in group C ( P<0.01 ) ; (2) Compared with control group, model groupdemonstrated evident inflammation in airway and surrouding, an increase of the depth of airway wall and the area of collagen deposition; In dexamethasone group , the inflammation had been obviously alleviated but the remodeling changes were not markedly improved; (3) The depth of airway epithium, smooth muscle, submucosa and the area of collagen deposition of model group...
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