Procaccino F, Reinshagen M, Hoffmann P, Zeeh J M, Lakshmanan J, McRoberts J A, Patel A, French S, Eysselein V E
Inflammatory Bowel Disease Center, Harbor-UCLA Medical Center, Torrance, California.
Gastroenterology. 1994 Jul;107(1):12-7. doi: 10.1016/0016-5085(94)90055-8.
BACKGROUND/AIMS: The role of epidermal growth factor (EGF) in the maintenance of mucosal integrity in the lower gastrointestinal tract is unknown. The aim of this study was to determine the effect of EGF in experimental colitis.
Colitis was induced with 2,4,6-trinitrobenzenesulfonic acid/ethanol enemas. Rats were pretreated with intraperitoneal administration of recombinant human EGF (600 micrograms/kg) or vehicle 1 hour before induction of colitis and daily thereafter until killed at 8 hours, 48 hours, and 1 week. A separate group received an identical dosage and administration of EGF or vehicle for 1 week with treatment initiated 24 hours after the induction of colitis. Colonic tissue was evaluated macroscopically, histologically, and for myeloperoxidase activity.
Pretreatment with EGF reduced microscopic erosions at 8 and 48 hours by 74% and 54%, respectively (P < 0.05). At 1 week, microscopic ulcerations and myeloperoxidase activity were reduced by 65% in the EGF-pretreated group (P < 0.05). No significant difference in macroscopic injury, histological damage, or myeloperoxidase activity was noted when EGF treatment was initiated after the induction of colitis.
Systemic EGF administration reduces mucosal damage and inflammation in a trinitrobenzenesulfonic acid/ethanol model of colitis in rats through a mechanism involving mucosal protection.
背景/目的：表皮生长因子（EGF）在维持下消化道黏膜完整性中的作用尚不清楚。本研究旨在确定EGF在实验性结肠炎中的作用。
用2,4,6-三硝基苯磺酸/乙醇灌肠诱导结肠炎。在诱导结肠炎前1小时，大鼠腹腔注射重组人EGF（600微克/千克）或赋形剂进行预处理，此后每天给药，直至在8小时、48小时和1周时处死。另一组在诱导结肠炎24小时后开始，接受相同剂量和给药方式的EGF或赋形剂治疗1周。对结肠组织进行宏观、组织学评估及髓过氧化物酶活性检测。
EGF预处理在8小时和48小时时分别使微观糜烂减少74%和54%（P<0.05）。在1周时，EGF预处理组的微观溃疡和髓过氧化物酶活性降低了65%（P<0.05）。在诱导结肠炎后开始EGF治疗时，在宏观损伤、组织学损伤或髓过氧化物酶活性方面未观察到显著差异。
在大鼠三硝基苯磺酸/乙醇诱导结肠炎模型中，全身性给予EGF通过一种涉及黏膜保护的机制减少黏膜损伤和炎症。
