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目的：观察大鼠肠缺血再灌注后肾脏内源性碱性成纤维细胞生长因子（ｂＦＧＦ）和转化生长因子β（ＴＧＦβ）基因与蛋白表达水平的变化，探讨ｂＦＧＦ和ＴＧＦβ促进损伤修复的分子调控机制。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４５分钟组、再灌注６小时组及再灌注２４小时组。ｂＦＧＦ和ＴＧＦβ基因表达用原位杂交方法检测，蛋白表达用免疫组织化学过氧化物酶标记的链酶卵白素（ＳＰ）染色方法测定。结果：肠缺血再灌注损伤后肾内源性ｂＦＧＦ和ＴＧＦβ基因和蛋白的表达水平均明显增高，于再灌注６小时达峰值，２４小时有所下降。结论：肠缺血再灌注损伤诱导了内源性ｂＦＧＦ和ＴＧＦβ的表达，可能是严重创伤后机体自身的一种保护机制
OBJECTIVE: To observe the expression of bFGF and TGFβ in kidney after intestinal ischemia-reperfusion (I / R) in rats, and to explore the effect of bFGF and TGFβ Regulatory mechanism. Methods: The rat model of superior mesenteric artery occlusion was used. The animals were randomly divided into sham operation group, ischemia 45 minutes, reperfusion 6 hours and reperfusion 24 hours. The expression of bFGF and TGFβ was detected by in situ hybridization. The protein expression was detected by streptavidin-peroxidase (SP) staining. Results: The expressions of endogenous bFGF and TGFβ mRNA and protein were significantly increased after intestinal ischemia-reperfusion injury, reaching the peak at 6 hours after reperfusion and decreasing at 24 hours. Conclusion: Gut ischemia-reperfusion injury induced the expression of endogenous bFGF and TGFβ, which may be a protective mechanism of the body itself after severe trauma