摘要
目的 :探讨细胞凋亡在烫伤鼠肺组织损伤中的作用及基因调控机制 ,为进一步阐明烫伤鼠肺组织损伤机制和在细胞凋亡水平防治烧伤后脏器损伤提供理论依据。方法 :采用原位末端标记 (TUNEL)法及免疫组织化学技术观察烫伤鼠肺组织细胞凋亡及肺组织 Fas/Fas L、核因子κB(NFκB) /IκB和 Bcl 2基因表达、鼠烫伤后肺组织通透性及 VE 钙黏附分子表达 ;电镜扫描肺组织血管内皮细胞连接的变化。结果 :1烫伤鼠肺组织细胞发生凋亡 ,尤其是肺泡上皮细胞和肺血管内皮细胞凋亡增加明显 ;2烫伤鼠肺组织对 99锝标记的亚锡喷替白蛋白通透性明显增加 ,同时肺组织血管内皮细胞 VE 钙黏附分子表达下降 ,与肺组织细胞凋亡呈平行关系 ;3烫伤鼠肺组织 Fas/Fas L 表达明显上调 ,Bcl 2表达明显下调 ,Fas/Fas L 表达的增加与肺组织细胞凋亡增加呈平行关系 ;4NFκB/IκB的表达与 Fas/Fas L表达相一致 ;5电镜扫描见肺组织血管内皮细胞连接增宽。结论 :鼠烫伤后肺泡上皮和肺血管内皮细胞发生凋亡 ,细胞凋亡参与了烫伤鼠肺组织损伤、通透性增加及内皮细胞连接损伤的发生过程 ;鼠烫伤后肺组织 Fas/Fas L、NFκB/IκB和 Bcl 2系统活化 。
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.
出处
《中国危重病急救医学》
CAS
CSCD
2002年第2期78-82,共5页
Chinese Critical Care Medicine
基金
国家自然科学基金重点课题资助项目 ( No.39830 40 0)
