The potential role and mechanism of cellular apoptosis in acute lung injury in scalded rats

Objective:To explore the potential role and mechanism of gene modulation of cell apoptosis in acute lung injury in scalded rats,and to provide theoretical basis for the prevention and treatment of postburn internal organ injury.Methods:Apoptosis of pulmonary parenchymal cells in scalded rats was observed with TdTmediated dUTP nick end labeling(TUNEL) method.The gene expression of Fas/FasL,nuclear factorκB (NFκB)/IκB,Bcl2,and VEcalcium adhesion molecules were determined in pulmonary tissues.The change in vascular endothelial conjunction of pulmonary tissue was observed by EM scanning.Results:①Apoptosis occurred in the pulmonary cells of scalded rats,particularly in alveolar epithelial and pulmonary vascular endothelial cells.②Pulmonary permeability in scalded rats was evidently increased when measured by 99 Tm labeled albumin.At the same time the expression of VEcalcium adhesion molecule in pulmonary vascular endothelial cells was decreased,and this was correlated with pulmonary cellular apoptosis.③In pulmonary tissue of scalded rats,expression of Fas/FasL was markedly upregulated while that of Bcl2 downregulated,and expression of Fas/FasL was correlated with increased pulmonary cellular apoptosis.④The expression of NFκB/IκB was in accordance with that of Fas/FasL.⑤Vascular endothelial conjunction in pulmonary tissue was widened when observed with EM scanning.Conclusions:Apoptosis could be found in the alveolar epithelial and pulmonary vascular endothelial cells following thermal injury,which might be related to the pathogenesis of acute lung injury,increased pulmonary microvascular permeability and interendothelial conjunction injury in scalded rats.The activation of pulmonary tissue Fas/FasL,NFκB/IκB and Bcl2 systems might be involved in the pathogenesis of the postburn lung injury and the signal transduction of pulmonary cell apoptosis.