| Objective: To observe the effect of hydrochloride penehyclidine,(Pneheydidine hydrochloride, PHCD) on the peroxisome proliferator-activated receptor-gamma (PPAR-y) and intercellular adhesion molecule-1(ICAM-1)in acute lung injury of rats, the protective Influence of hydrochloric acid penehyclidine on acute lung injury will be discussed.Methods: according to the random number table, a group of healthy adult SD rats32, weighting (220±10) g, male or female, is randomly divided into four groups (n=8), respectively, for the normal group, hydrochloric acid injury group, pretreatment and treatment group. The use of Ph=1.25hydrochloric acid, according to the dose of1.2ml/kg injected rat tracheal preparation of gastric contents aspiration induced acute lung injury model. Pretreatment Rats were given PHCD1.Omg/kg1hour before modeling, while the treatment group were given the same dose one hour after the successful modeling.4hours after successful modeling, the rats were made intraperitoneal injection of chloral hydrate anesthesia, and arterial blood was collected via the aorta, as well as determination of arterial blood gas indicators, and then animals were sacrificed. Right lower lung were fexed by10%formalin for two weeks, and went through dehydration, paraffin embedding, made of sections, HE staining. Determination of the PPAR-y and ICAM-1expression in lung tissue were measured by immunohistochemical methods. Statist ical analysis were done by SPSS16.0software, and measurement data were expressed as mean±standard deviation.(P<0.05) difference was statistically significant.Results:1. The amount of arterial PaO2in Injury rats is (65.62±6.24) mmHg, compared with the normal group and arterial blood (102.29±8.55) mm Hg, significantly decreasing (P<0.01). Pretreated group and the treated rats arterial PaO2(84.38±7.20) mmHg and (77.26±7.83) mmHg, compared with the injured group, significantly increased (P<0.01).And compared with the treatment group,the pretreatment group, arterial PaO2improved significantly (P<0.05).2.H E Stained found:normal lung tissue structural integrity of the alveolar structure is clear, uniform size, the alveolar wall and interstitial edema and inflammatory cell infiltration. Injury were observed in lung tissue diffuse congestion, a high degree of edema, alveolar organizational structure destruction, widened pulmonary interval, aggregation of pulmonary and quality of alveolar inflammatory cells, alveolar collapse and a large number of red blood cells are visible. Pr etreated group did not have obviously visible pulmonary edema, and pulmonary interval thickening is lighter, more complete alveolar structure, collapse is not obvious and a few inflammatory cells gathered. More complete treatment group had alveolar structure and inflammatory cell infiltration, alveolar mild edema, pulmonary interstitial and alveolar saw a certain number of inflammatory cells. Under a microscope, normal lung tissue saw a large number of PPAR-γ expression-positive vascular endothelial cells, alveolar epithelial cells and macrophages cells. Injury lung tissue expression of PPAR-y-positive cells were significantly reduced. A certain amount of PPAR-y expression-positive cells can be seen in Pretreatment and treatment groups, but more in the pretreatment group than the treatment group. Alveolar septa of normal group showed no ICAM-1expression in the endothelial cell surface and alveolar epithelial cells. Alveolar interval, vascular endothelial cells and alveolar epithelial cells of the injury showed a large number of brown or dark brown particles. In the pretreatment and treatment groups, alveolar septa, vascular endothelial cells and alveolar epithelial cells can also find varying amounts of brown or dark brown particles, but the number was significantly reduced than the injured group, and the pretreatment group was less than the treatment group. Compared with normal group, PPAR-y expression of injured group was decreased, ICAM-1expression was significantly increased (P<0.01).Compared with the injured group, while in the pretreatment group, PPAR-y expression was elevated expression of ICAM-1expression decreased (P<0.01). Compared with the injured group, treatment group, PPAR-y increase the expression of ICAM-1expression decreased (P<0.01). Compared with treatment group, the pretreatment group, PPAR-y increase and the expression of ICAM-1expression decreased (P<0.05).Conclusion:penehyclidine hydrochloride on acute lung injury act as the role of prevention and treatment effect on the disease before the application effect is more pronounced, and its mechanism may be related to increasing the body PPAR-y expression and inhibitating the ICAM-1expression. |
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