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探讨肾缺血再灌流损伤修复过程中颌下腺、胰腺、肾脏产生的表皮生长因子（ＥＧＦ）的作用及作用机制。方法选用大鼠右肾切除、左肾缺血６０ｍｉｎ继之再灌流不同时间模型，观察颌下腺切除后对肾功能和形态恢复的影响。用免疫组化和ＷｅｓｔｅｒｍＢｌｏｔ方法观察肾缺血再灌流损伤修复过程中肾组织增殖细胞核抗原（ＰＣＮＡ），胰腺、颌下腺、肾脏和血清ＥＧＦ以及肾组织ＥＧＦ受体（ＥＧＦＲ）表达的变化。结果颌下腺切除后，损伤后的肾功能和肾组织形态结构恢复到正常的时间明显延长。ＰＣＮＡ免疫组化显示，６０ｍｉｎ肾缺血再灌流２４ｈ出现再生，再灌流３ｄ再生修复达到高峰，再灌流７ｄ基本消失。与此相对应，颌下腺、胰腺在再灌流１、３ｄ时ＥＧＦ表达明显增强，血清ＥＧＦ含量增多，肾组织ＥＧＦＲ表达明显增强；再灌流７ｄ时，颌下腺、胰腺ＥＧＦ表达、血清ＥＧＦ含量及肾组织ＥＧＦＲ表达均基本恢复正常。结论颌下腺、胰腺所产生的ＥＧＦ在损伤后肾小管上皮的修复中可能起重要作用，ＥＧＦ可能通过ＥＧＦＲ介导机制促进损伤肾小管上皮的修复
To investigate the effect and mechanism of epidermal growth factor (EGF) produced by submandibular gland, pancreas and kidney in the process of renal ischemia reperfusion injury repair. Methods Right kidney resection, left renal ischemia 60min followed by reperfusion different time models were observed after submandibular gland resection of the renal function and morphological recovery. Immunohistochemistry and WestermBlot method were used to observe the changes of PCNA, pancreas, submandibular gland, kidney and serum EGF and the expression of EGFR in renal tissue during renal ischemia / reperfusion injury. Results After submandibular gland resection, the renal function and the morphological structure of renal tissue restored to normal after the injury were significantly prolonged. PCNA immunohistochemistry showed that after 60min of renal ischemia-reperfusion, regeneration appeared, and the peak of reperfusion was reached after 3-day reperfusion, disappearing 7d after reperfusion. Correspondingly, the expression of EGF in submandibular gland and pancreas was significantly increased at 1 and 3 days after reperfusion, and the content of EGF in serum increased, and the expression of EGFR in renal tissue was significantly increased. On the 7th day after reperfusion, the expression of EGF in submandibular gland and pancreas, The expression returned to normal. Conclusion The EGF produced by submandibular gland and pancreas may play an important role in the repair of renal tubular epithelial cells after injury. EGF may promote the repair of injured renal tubular epithelial cells through EGFR-mediated mechanism