严重缺氧后心肌细胞损害敏感性的分子机制  

Molecular mechanism of the sensitivity of myocardial cell injury after severe hypoxia

作　　者：王水明[1] 刘友生[1] 陈锐[1] 

机构地区：[1]第三军医大学西南医院病理研究所,重庆400038

出　　处：《中华烧伤杂志》2003年第3期134-136,共3页Chinese Journal of Burns

基　　金：国家重点基础研究发展规划资助项目 (G19990 5 42 0 2 )

摘　　要：目的　探讨严重缺氧后心肌细胞损害敏感性的分子机制。方法　以包含 4 0 96条小鼠基因的DNA芯片 ,检测严重缺氧 6h的大鼠心肌和骨骼肌细胞之间的差异表达基因。结果　严重缺氧 6h后 ,12 5条基因在骨骼肌细胞中高表达 ,111条基因在心肌细胞中高表达。其中 ,编码凋亡活化因子Mtd、补体C3、血管细胞粘附分子 1(VCAM 1)、β 整合素及脂多糖结合蛋白 (LBP)等的基因在心肌细胞中高表达。结论　严重缺氧 6h后 ,凋亡活化及炎症介质的产生在心肌细胞敏感性损害中发挥着重要作用。Objective To explore the molecular mechanism of the sensitivity of myocardial cell injury after severe hypoxia. Methods Differential expression of the genes in rat myocardium and skeletal muscles after severe hypoxia for 6 hours was determined by DNA chip containing 4096 mice genes. Results There were high expressions of 125 genes in skeletal muscles and 111 genes in myocardial cells after 6 hours of severe hypoxia. Among them, high expression genes in myocardial cells included those encoding apoptosis activator Mtd, complement C3, vascular cell adhesion molecule-1, integrin beta subunit and lipopolysaccharide binding proteins(LBP). Conclusion Activation of apoptosis of myocardial cells and inflammatory mediators played important roles in myocardial cell injury after 6-hour severe hypoxia.

关 键 词：缺氧 心肌细胞 敏感性 分子机制 基因芯片 

分 类 号：R363[医药卫生—病理学]