摘要
目的:研究缺血再灌注损伤致肠道内源性碱性成纤维细胞生长因子(bFGF)和转化生长因子β(TGFβ)基因表达的变化特征与规律,探讨这两种因子基因表达变化与肠道修复的关系。方法:利用大鼠肠系膜上动脉夹闭45分钟与再灌注6小时与24小时动物模型,用原位杂交与逆转录聚合酶链式反应技术检测两种因子mRNA表达水平、定位及时相变化。结果:在正常小肠粘膜,bFGF与TGFβ的mRNA表达均为弱阳性,主要位于小肠绒毛的固有层。缺血45分钟,小肠粘膜bFGFmRNA的阳性信号消失,而TGFβmRNA的表达量却明显增加;再灌注6小时与24小时,两种因子mRNA表达量接近于伤前。结论:缺血再灌注损伤可导致肠道内源性bFGF与TGFβ基因表达的改变。
Objective:To investigate the changes in basic fibroblast growth factor (bFGF) and transforming growth factor β( TGFβ) gene expression in intestine after ischemiareperfusion injury,and their possible role in the pathogenesis of internal organ repair.Methods:Wistar rats were subjected to superior mesenteric artery occlusion (45 minutes) followed by reperfusion (24 hours),and 16 animals were divided into 4 groups as follows:normal,ischemia (45 minutes),ischemia (45 minutes) plus reperfusion (6 hours),and ischemia (45 minutes) plus reperfusion (24 hours).After being scarifed on schedule,the biopsies of small intestines were harvested for gene expression by in situ hybridization and reverse transcription polymerase chain reaction (RTPCR).Results:Both of bFGF and TGFβ mRNA were slightly expressed in normal small intestines,but the expression signal was only localized in submucosa.After 45 minutes ischemia insult,the positive signal of bFGF mRNA was reduced when compared with the normal group,however,the TGFβ mRNA expression was increased significantly.At 6 and 24 hours after reperfusion,the gene expression of both growth factors returned to baseline values.Additionally,similar results in bFGF and TGFβ mRNA were obtained by RTPCR and in situ hybridization.Conclusions:Our results suggest that intestinal ischemia and reperfusion injury results in the gene expression in both growth factors,which may be associated with the pathophysiological alterations and gut repair following acute ischemiareperfusion.
出处
《中国危重病急救医学》
CSCD
1998年第8期459-462,共4页
Chinese Critical Care Medicine
基金
国家杰出青年科学基金
关键词
缺血
再灌注损伤
bFCF
TGFΒ
基因
ischemia and reperfusion\ \ gut\ \ transforming growth factor β\ \ basic fibroblast growth factor\ \ gene