目的　新生儿窒息可引起糜烂、溃疡和出血等胃肠粘膜损伤。既往成年动物研究发现表皮生长因子 (EGF)及其受体 (EGFR)在急性胃肠粘膜损伤后的修复过程中发挥重要作用。该文旨在探讨EGF和EGFR在宫内窒息新生鼠胃粘膜的表达及其在胃粘膜损伤后修复过程中的作用。方法　用孕足 2 1d大鼠制作成宫内窒息模型 ,将剖宫产后存活的窒息组和对照组新生鼠在出生 0、2 4、4 8和 72h断头处死 ,留取胃标本。应用免疫组化方法和反转录 -多聚酶链反应动态监测新生鼠胃粘膜EGF、EGFR和EGFRmRNA的表达 ,同时观察胃组织形态学改变。结果　 (1 )窒息组新生鼠出现胃粘膜损伤 ,于生后 4 8h损伤最重 ,之后开始恢复。 (2 )对照组新生鼠胃粘膜有较弱的EGF和EGFR表达 ,各时间点差异无显著性 (P >0 .0 5 )。 (3)窒息组新生鼠胃粘膜EGF和EGFR的表达随生存时间增加而增强 ,在 4 8h达高峰之后开始下降 ,生后 2 4 ,4 8,72h胃粘膜EGF表达与对照组同时相比较 ,差异均有显著性 (P <0 .0 1或 0 .0 5 )。 (4 )窒息组新生鼠胃粘膜EGFRmRNA的表达于 2 4h达高峰 ,较对照组同时间点相比增加 ,差异非常显著性 (P <0 .0 1 ) ,之后开始减少。结论　EGF和EGFR可能在窒息后新生鼠胃粘膜损伤后的修复过程中发挥重要作用

Objective Neonatal asphyxia may induce acute gastrointestinal injuries such as erosion, ulcer, bleeding and so on. Recent investigations have shown that epidermal growth factor (EGF) and its receptor (EGFR) play an important role while participating in the reparation of acute gastrointestinal injury in adult animals. This paper aims at studying the expressions of EGF and EGFR in gastric mucosa of neonatal rats with intrauterine asphyxia as well as their roles in the reparation of gastric mucosa lesions. Methods Wistar rats, 21 days pregnant, were used to establish animal models of intrauterine asphyxia. The surviring pups of the Asphyxia group and the pups without asphyxia (Control group) were sacrificed by decapitation at 0, 24, 48, 72 hrs after birth and gaster specimens were collected. The expressions of EGF, EGFR and EGFR mRNA in the gastric mucosas were assayed by immunohistochemistry and reverse transcription polymerase chain reaction (RT PCR) and the histology of gastric mucosas were observed. Results (1) The gastric mucosa lesions of neonatal rats were found in the Asphyxia group and became more and more serious untill a peak was reached 48 hrs after birth. (2) Low expressions of EGF and EGFR could be detected in the gastric mucosas of rats in the Control group, and there were no differences among various time points. (3) The expressions of EGF and EGFR in the gastric mucosas of neonatal rats in the Asphyxia group increased with time and reached the peak 48 hrs after birth. The EGFR expressions at 24, 48 and 72 hrs in the Asphyxia group were significantly higher than those of the Control group (P< 0.01 or 0.05 ). (4) The expression of EGFR mRNA in the gastric mucosa of neonatal rats in the Asphyxia group reached a peak 24 hrs after birth and was higher than that of the Control group (P< 0.01 ). Conclusions EGF and EGFR may play an important role in the reparation of gastric mucosa lesions of neonatal rats with intrauterine asphyxia.