Egger B, Procaccino F, Sarosi I, Tolmos J, Büchler M W, Eysselein V E
Harbor-UCLA Medical Center, Division of Gastroenterology, Torrance, California 90502, USA.
Dig Dis Sci. 1999 Apr;44(4):836-44. doi: 10.1023/a:1026642715764.
Keratinocyte growth factor (KGF) is emerging as an important mediator of mucosal defense and repair in the colon. The aim of the present study was to evaluate and further characterize the effects of exogenous KGF administration utilizing the dextran sodium sulfate (DSS) model of colitis in mice. Colitis was induced via oral administration of DSS (5 g/100 ml) to Balb/c mice for eight days. Intraperitoneal administration of KGF (5 mg/kg, once daily) or vehicle (VEH) was initiated 1 hr prior to the induction of the colitis (N = 10, each group). Mucosal injury of the entire colon was histologically assessed and graded. An approximately fourfold reduction in the crypt damage score was noted in the KGF group when compared to controls (VEH) (2.8 +/- 1.03 and 11.4 +/- 0.78, respectively). The significant reduction of mucosal injury in KGF treated mice confirms that KGF is a key mediator maintaining the integrity of the colonic mucosa.
角质形成细胞生长因子（KGF）正成为结肠黏膜防御和修复的重要介质。本研究的目的是利用葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎模型，评估外源性KGF给药的效果并进一步进行特征描述。通过给Balb/c小鼠口服DSS（5 g/100 ml）持续8天来诱导结肠炎。在诱导结肠炎前1小时开始腹腔注射KGF（5 mg/kg，每日1次）或赋形剂（VEH）（每组N = 10）。对整个结肠的黏膜损伤进行组织学评估和分级。与对照组（VEH）相比，KGF组的隐窝损伤评分降低了约四倍（分别为2.8±1.03和11.4±0.78）。KGF治疗小鼠的黏膜损伤显著减轻，证实KGF是维持结肠黏膜完整性的关键介质。
