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Background bronchial asthma (hereinafter referred to as asthma) is characterized by chronic airway inflammation caused by eosinophils, mast cells, lymphocytes and other cells and cell components, airway morphology changes reflect the structure changes, airway remodeling (airway remodeling). Now commonly recognized, including the shedding of epithelial cells, thickening of the basement membrane, expansion and proliferation of blood vessels, airway smooth muscle proliferation, mucus gland and goblet cell hyperplasia, collagen deposition. Process of vascular to become all levels of the network by endothelial cells and pericytes and smooth muscle cells from the original lumen angiopoietin of -1 (angiopoietin-1, Ang-1) and its receptor Tie-2 from a very important role. Ang-1 is the muscle of secreted ligands, plays an important role in physiological and pathological angiogenesis process. It is reported that Ang-1 regulates the connection between the endothelial cell adhesion molecules and cells, but also prevent the vascular endothelial growth factor (vascular endothelial growth factor, VEGF) or vascular leakage caused by inflammatory mediators which play an anti-inflammatory effect. By endothelial specific receptors Tie-2 activation of phosphodiesterase, phosphatidyl inositol 3 'kinase and tyrosine kinase, significantly inhibited VEGF-induced eosinophil chemoattractant. Therefore, Ang-1 may be induced microvascular leakage and inflammation treatment. Ang family of four forms, Ang-1, Ang-2, Ang-3 and Ang-4, Ang-1 is widely expressed in adults in a variety of tissues. At present, most research has focused on Ang-1 and Ang-2. Tie is a vascular endothelial cell specific tyrosine kinase receptor, Tie-1, Tie-2 two Since Tie-1 receptor ligands have not yet found, so most research has focused on the Tie-2 receptors. Tie-2 expression in vascular endothelial cells (endothelial cells, ECS) and early hematopoietic cells. Not yet seen Ang-1 and its receptor Tie-2 in asthma abroad just begun. Asthma model copied by stimulating this experiment using the immunohistochemistry (immnohistochemical) detects Ang-1 and its receptor Tie-2 in the normal group, asthma group and the intervention group between the different groups of airway wall expression changes, using computer pathological picture Road re-like analysis system to analyze the relationship between the rats airway wall thickness and the above two factors, designed to explore the role of Ang-1 and its receptor Tie-2 in the process of the development of asthma pathophysiology asthma gas The plastic provides treatment and prevention of new ideas. Materials and Methods 45 healthy female SD rats (body weight J10 ± 10g, 5-6-week-old) were randomly divided into the following groups: (1) control group: intraperitoneal injection of 1 ml of saline, and inhalation of saline. (2) The model group: Preparation of asthma model, OVA (chicken egg albumin) sensitization, 1% OVA inspire. 1d pet rats by intraperitoneal injection 1ml 10% OVA suspension (containing 1 ml saline, 100 mg of aluminum hydroxide 100mgOVA) sensitization, 8d, 15d each repeat, 16d start with OVA excitation, the rats placed in a specially sealed glass container, using an ultrasonic nebulizer sprayed into the 1% OVA, every other day, every 20min, excited 20 times. (3) dexamethasone intervention group: excited before 30min 2mg/kg intraperitoneal injection of dexamethasone solution, the other with the model group. Rats in each group, respectively, the last challenge within 24h after intraperitoneal anesthesia with sodium phenobarbital (100mg / only) to death. The structure of the airway, HE staining, immunohistochemical staining using computer pathological image analysis systems analysis groups of rat airway wall expression of Ang-1 and its receptor Tie-2 positive percentage measured 10 × 20 under airway wall thickness, and to analyze the relationship between Ang-1 and Tie-2, both the thickness of airway, statistical analyzes were performed using SPSS (11.0) statistical software to calculate the results to the arithmetic mean ± standard deviation ((?) ± s ). Group, homogeneity of variance test using single-factor analysis of variance (one-way ANOVA), and linear correlation analysis to α = 0.05 level of inspection, P <0.05 for the difference was significant. Results 1. Airway wall thickness measured airway thickness compared with control group, model group (47.266 ± 2.531) and intervention group (39.267 ± 2.011) compared with the control group (36.533 ± 2.166) and a significant increase (P <0.01), model group (47.266 ± 2.531) compared to the intervention group increased significantly (P <0.01). 2. Ang-1 and its receptor Tie-2 expression in rat airway wall in the control group and the intervention group, Ang-1 and its receptor Tie-2 weaker expression in airway epithelial cells, smooth muscle cells and vascular endothelial cells and so on. In the model group, Ang-1 and its receptor Tie-2 is strongly expressed in airway epithelial cells, smooth muscle cells and endothelial cells. Ang-1 model group (103.9487 ± 8.2914) and the control group (76.0320 ± 3.7728) and the intervention group (90.6180 ± 5.2339) comparison, expression were significantly with increased (P <0.01), the intervention group and the control group of also increased (P < 0.01). Tie-2 model group (99.2307 ± 8.1913) and the control group (75.3153 ± 3.7321) and intervention group (86.6633 ± 3.7321) comparison, expression were significantly with increased (P <0.01), the intervention group and the control group of also increased (P < 0.01). 3. Ang-1 and its receptor Tie-2 and airway wall thickness between the correlation analysis of Ang-1 and its receptor Tie-2 expression and airway wall thickness was significantly correlated (r Ang-1 < / sub> = 0.719 the r Tie-2 = 0.746, P <0.01), Ang-1 and its receptor Tie-2 also showed a significant positive correlation (r Angl-Tie-2 = 0.742, P <0.01). Conclusion 1. Ang-1 and its receptor Tie-2 in the airway is widely expressed. 2. Asthmatic rats airway wall Ang-1 and its receptor Tie-2 expression was significantly increased, and airway wall thickness are closely related. 3. Ang-1 and its receptor Tie-2 may inhibit the the asthmatic airway reconstruction process.
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