Protective effect of ischemic postconditioning on rat models of lung ischemia/reperfusion injury / 中国组织工程研究

ABSTRACT

BACKGROUND:Pneumonectomy, extracorporeal circulation, lung transplantation and pulmonary embolism can cause ischemia/reperfusion injury of lung tissue. Lung ischemia/reperfusion injury is an important factor of lung function disorders after lung transplantation. OBJECTIVE:To analyze the effect of ischemic postconditioning on rat models of lung ischemia/reperfusion injury. METHODS:Twenty-four male SD rats were randomly divided into sham, ischemia/reperfusion and ischemic postconditioning groups (n = 8 rats/group) to establish the lung ischemia/reperfusion injury model. The rats in the sham group were only subjected to separation of the hilum of left lung and pulmonary arteries and veins, without blocking. The rats in the ischemia/reperfusion group were subjected to another 2 hours of reperfusion after 1 hour of lung ischemia. The rats in the ischemic postconditioning group were first subjected to 30 seconds of lung ischemia and 30 seconds of reperfusion for three times, and then to 2 hours of reperfusion. After the experiment, the specimens of lung tissue were obtained to detect the wet/dry weight ratio of lung tissue, activities of superoxide dismutase, malondialdehyde and myeloperoxidase, the contentsof inflammatory cytokines tumor necrosis factor α, interleukin-1β and interleukin-6, and the histopathological changes of lung tissue were observed. RESULTS AND CONCLUSION:Compared with the sham group, the wet/dry weight ratio of lung tissue, activities of myeloperoxidase and myeloperoxidase, the levels of tumor necrosis factor α, interleukin-1β and interleukin-6 were significantly increased (P < 0.05) in the ischemia/reperfusion and ischemic postconditioning groups, however, the increase levels of these indices were not significant in the ischemic postconditioning group, and the contents and activities in the ischemic postconditioning group were al significantly decreased (P < 0.05) compared with those in the ischemia/reperfusion group. In the ischemia/reperfusion and ischemic postconditioning groups, the activity of superoxide dismutase was obviously lower than that in the sham group, however, the activity of superoxide dismutase in the ischemic postconditioning group was obviously higher than that in the ischemia/reperfusion group. Pathological examination showed that thickened alveolar wal, edema and a large amont of inflammatory cel infiltrations were observed in the lung tissue of rats in the ischemia/reperfusion group. The degrees of alveolar wal thickening and edema in the lung tissue of rats in the ischemic postconditioning group were mild compared with the ischemia/reperfusion group, and in addition, some inflammatory cels were infiltrated. The histopathological scores of lung tissue in the ischemic postconditioning group were lower than those in the ischemia/reperfusion group. These results suggest that ischemic postconditioning plays its protective role on rat models of ischemia/reperfusion injury by inhibiting inflammatory cel accumulation, oxygen free radical production and pro-inflammatory cytokine release after ischemia/reperfusion injury.