ABSTRACT
Objective To investigate the effects of naloxone (Na) on pneumocyte apoptosis and expression of heme oxygenase-1 (HO-1) during ischemia reperfusion injury of lung in rats. Method Forty-two male Sprague-Dawley rats were made models of ischemia reperfusion injury of unilateral lung, and were randomly( random number) divided into three groups: sham operation group (Sh group), ischemia reperfusion group (IR group) and naloxone group (Na group). The hilus of lung was clamped for 45 minutes and the clamp was taken off to build the I/R model. After 3-6 hours reperfusion, naloxone in dose of 1 mg/kg was injected intra-peritoneally in rats of Na group. The rate of cell apoptosis in lung tissue was detected with the way of Annexin-V-PI in flow cy-tometer. The wet to dry weight ratio (W/D) of lung tissue was measured. The expression of HO-1 in lung was measured by using RT-PCR and the ultra-structure change of lung tissue was observed under electron microscope. Results The rate of pneumocyte apoptosis and W/D ratio of lung tissue were significantly higher in IR group than in Sh group (P < 0.01), and the rate of pneumocyte apoptosis and W/D ratio of lung tissue were negatively correlated with the expression of HO-1 mRNA in lung tissue. Compared with IR group, the rate of cell apoptosis and W/D ratio were lower and the expression of HO-1 mRNA was higher in Na group (P < 0.01). The ultra- structure changes of lung tissue were lessened in Na group than in IR group. Conclusions During early period of lung IR injury, HO-1 induced by naloxone can inhibit the cellular apoptosis and protect the lung tissue.
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.