Lung transplantation is an important consolidated, safe and effective therapeutic alternative widely used as a treatment for severe diseases in the advanced stage. The main goal for transplantation is to prolong and improve the quality of life of patients. The experimental models are important tools to help the understanding of pathophysiological phenomena, medication action or changes from specific interventions. The process of encephalic death involves a series of immunopathological changes that have a deleterious effect on the organ. The process triggers a cascade of events such as: hemodynamic, hormonal, metabolic and inflammatory changes. Studies in small animals demonstrate that during the process of brain death there is a systemic release of inflammatory cytokines such as IL-1, IL-6, TNF-± and INF-¥. The increase of these cytokines in the donor may contribute to the progressive deterioration of graft function associated with vascular and interstitial morphological changes in organ reperfusion .NF-kB is a transcription factor consisting of two protein subunits: p50 and p65. It is a member of the family of redox-sensitive transcription factors present in endothelial cells, vascular smooth muscle cells (VSMC), macrophages and lymphocytes. It remains inactive in the cytoplasm when bound to the inhibitory proteins known as IkB (kappa B inhibitor). In summary, the IkBs prevent NF-kB from detaching from the cytoplasm and into the nucleus of the cell. In this study we aimed to describe the inflammatory process of lungs submitted to thalidomide treatment in an experimental model of brain death.
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