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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 observe the effects of exogenous basic fibroblast growth factor (bFGF) on the expression of liver fibroblast growth factor (bFGF) and basic fibroblast growth factor receptor (FGFR1) in rats with ischemia-reperfusion, Molecular mechanisms of visceral injury repair. Methods: The rat model of superior mesenteric artery occlusion was used. The animals were randomly divided into sham group, ischemia group, exogenous bFGF group and untreated reperfusion group for 6, 24 and 48 hours. The expression levels of bFGF and FGFR1 were determined by immunohistochemical SP method. Results: The expression levels of endogenous bFGF and FGFR1 were significantly increased after ischemia-reperfusion injury, reaching the peak at 6 hours and 24 hours after reperfusion, respectively, and then decreased after 48 hours. Application of exogenous bFGF treatment, histological damage was significantly improved at the same time, bFGF expression was significantly higher than non-treatment group, while the expression level of FGFR1 no change. CONCLUSION: Ischemia-reperfusion injury induces the expression of endogenous bFGF and FGFR1, whereas exogenous bFGF regulates tissue repair after liver injury by up-regulating the expression of endogenous bFGF or binding itself with FGFR1.