Apoptosis in lung ischemia-reperfusion studies in progress.docVIP

 PAGE \* MERGEFORMAT 23 Apoptosis in lung ischemia-reperfusion studies in progress [Keywords:] lung ischemia reperfusion; apoptosis Ischemia-reperfusion (Ischaemia-reperfusion, IR) induced lung damage, cardiopulmonary surgery, particularly in lung transplantation is a major clinical problem, and as the application of cardiopulmonary bypass, postoperative pulmonary dysfunction is common, even patients thus result in life-threatening. Early researches focus on the lung tissue damage caused by cell necrosis, until recently of lung ischemia-reperfusion injury (Lung Ischaemia-reperfusion Injury, LIRI) mechanism of apoptosis induced by gradually was valued by the people. apoptosis process is strictly controlled process multiple genes, such as Bcl-2 family, Caspase family, cancer genes, such as C-myc, tumor suppressor gene P53 and so on. LIRI in recent years is the pathological mechanism of apoptosis in and Bcl-2, Bax, caspase-3, etc., in which the role of regulatory genes are reviewed. 1 cells and lung ischemia-reperfusion injury Ischemia-reperfusion injury in the lung in addition to direct cellular necrosis, apoptosis is the basic form of cell death. Lack of oxygen in the ischemic stage, necrosis of cells majority, and the cells were mostly in the reperfusion stage. Fischer is equal to the transplanted lung after reperfusion pathological biopsy, apoptosis was significantly increased and associated with the reperfusion time [1]. Stammberger that severe reperfusion injury occurred early in the process of lung transplantation [2]. ischemia cause apoptosis of lung cells slightly increased 2 hours after reperfusion lung cell apoptosis peak. The discovery of such Omasa reperfusion injury secondary to the number of apoptotic cells and cells with the pulmonary shunt fraction was significantly correlated with oxidative damage [3]. apoptotic process a series of characteristic changes. One of the most important thing is the genome of the apoptosis process of fragme