摘要
目的：通过观察外源性碱性成纤维细胞生长因子（ｂＦＧＦ）对缺血 再灌注大鼠肝脏内源性ｂＦＧＦ及碱性成纤维细胞生长因子受体（ＦＧＦＲ１）表达水平的影响，探讨ｂＦＧＦ调控内脏损伤修复的分子机制。方法：采用大鼠肠系膜上动脉夹闭模型，将动物随机分为假手术组、缺血即刻组、外源性ｂＦＧＦ治疗组及未治疗的再灌注６、２４ 和４８小时组。ｂＦＧＦ和ＦＧＦＲ１ 的表达水平采用免疫组织化学ＳＰ方法测定。结果：缺血 再灌注损伤后内源性ｂＦＧＦ和ＦＧＦＲ１ 表达水平均明显提高，分别在再灌注６小时和２４ 小时达峰值，４８小时后下降。应用外源性ｂＦＧＦ治疗后，在组织学损伤得到明显改善的同时，ｂＦＧＦ表达水平也较非治疗组明显提高，而ＦＧＦＲ１ 的表达水平无变化。结论：缺血 再灌注损伤诱导了内源性ｂＦＧＦ和ＦＧＦＲ１ 的表达，而外源性ｂＦＧＦ可能通过上调内源性ｂＦＧＦ的表达或其自身与ＦＧＦＲ１ 结合，调控肝损伤后的组织修复。
Objective:To investigate the effect of exogenous basic fibroblast growth factor (bFGF) on he patic endogenous bFGF and FGF receptor (FGFR 1) expression following intestinal ischemiareperfusion injury,and to explore its molecular regulation mechanisms with regard to promoting tissue repair.Methods:Male Wistar rats were subjected to superior mesenteric artery occlusion followed by reperfusion.Animals were randomly divided into control,end of ischemia,6,24 and 48 hours after reperfusion with or without exogenous bFGF treatment.FGFR 1 and bFGF expressions were examined by immunohistochemical methods.Results:bFGF and FGFR 1 expression were induced by ischemiareperfusion injury,peaking at 6 and 24 hours and decreasing at 48 hours after reperfusion,respectively.Treatment with exogenous bFGF markedly attenuated pathological damage,and enhanced bFGF expression compared with nontreatment group,but had no significant influence on FGFR 1 expression.Conclusions:Hepatic endogenous bFGF and FGFR 1 expression could be induced by ischemia injury,and it seems that exogenous bFGF promotes tissue repair associated with hepatic injury via upregulation of endogenous bFGF expression or by combinating with FGFR 1.
出处
《中国危重病急救医学》
CSCD
1999年第12期734-736,共3页
Chinese Critical Care Medicine
基金
国家杰出青年基金
关键词
组织修复
BFGF
FGFR1
缺血再灌注损伤
hepatic ischemiareperfusion
basic fibroblast growth factor
fibroblast growth factor receptor
tissue repair
