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Effect of ischemic preconditioning on pneumocyte apoptosis and the expression of HSP70 during pulmonary ischemia-reperfusion injury in rats / 中华急诊医学杂志
Chinese Journal of Emergency Medicine ; (12): 1143-1146, 2008.
Article in Chinese | WPRIM | ID: wpr-397681
ABSTRACT
Objective To investigate the effects of ischemic preconditioning on pneumocyte apoptosis and the expression of HSFT0 after lung isehemia-reperfusion(I/R) in rats and discuss its possible mechanism of extenu-ating ischemia-repedusion injury. Method Thirtysix male Sprague-Dawley rats were randomly divided into three groups [ sham operation(SO ) group, ischemia-teperfusion(L/R) group, and ischemic preconditioning(IP) group],twelve in each group. Lung croas-clamping was used to build the L/R model. In IP group, three cycles of 5-minute-ischemia + 5-minute-reperfusion were given to the pulmonary artery before the procedure. Sham operation rats had a thoracotomy only. Two hours(or five hours) reperfusion was given to both L/R and IP group. Tenninal-deoxynucleotidyl Transferase Mediated d-UTP Nick End Labeiing(TUNEL) was used to evaluate apoptosis. Expression of HSP/0 in lung was observed by immunohistochemical stain and image analysis. Index of quantitative assessment of histologic lung injury(IQA), wet to dry weight ratio(W/D) were measured. The pathological change of lung tissue was observed under both hght and electron microscopy. Statistical analysis was carried out by One-way Anova. Scheffe test was used for intragroup comparison. Results The apoptosis index and expression of HSP70、W/D,IQA of hng tissue in I/R group were higher than those in the sham operation group (P<0.01). Compared with the L/R group, the apoptosis index and expression of HSP70, W/D, IQA of lung tissue significantly decreased (P<0.01), the levels of expression of HSPTO increased significantly in IP group ( P<0.01 ). The pathological and ultrastructure change of lung tissue was better in IP group than those in I/R group. Condusions Ischemic preconditioning can extenuate lung I/R injury by the possible mechanism of increasing the expression of HSPT0 which inhibits the apoptosis during lung I/R injury.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Emergency Medicine Year: 2008 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Emergency Medicine Year: 2008 Type: Article