Paimela H, Goddard P J, Carter K, Khakee R, McNeil P L, Ito S, Silen W
Department of Surgery, Beth Israel Hospital, Boston, Massachusetts.
Gastroenterology. 1993 May;104(5):1337-45. doi: 10.1016/0016-5085(93)90342-a.
Rapid re-epithelialization after superficial gastric mucosal injury is caused by migration of persisting viable epithelial cells. Basic fibroblast growth factor (bFGF) has been reported to enhance the healing of experimental duodenal ulcer, but its mode of action is unclear. The present experiments examine whether an effect of bFGF on restitution might contribute to such healing.
Paired halves of bullfrog fundic gastric mucosa in Ussing chambers were injured by luminal exposure to 1 mol/L NaCl for 10 minutes.
Luminal protamine or suramin, both known to interfere with endogenous bFGF, significantly inhibited electrophysiological recovery at neutral luminal pH (pHL). Luminal sucrose octasulfate, which prevents acid degradation of bFGF, and an exogenous, acid-resistant form of bFGF allowed electrophysiological recovery at a pHL of 3.0 that completely prevented restitution in control tissues. Electrophysiological recovery correlated well with morphological restitution. The presence of endogenous bFGF in normal and restituting bullfrog mucosa was confirmed by positive staining with a monoclonal antibody.
It is concluded that rapid epithelial repair after surface injury is at least in part mediated by bFGF.
浅表性胃黏膜损伤后上皮细胞的快速重新上皮化是由存活的上皮细胞迁移引起的。据报道，碱性成纤维细胞生长因子（bFGF）可促进实验性十二指肠溃疡的愈合，但其作用方式尚不清楚。本实验旨在研究bFGF对修复的影响是否有助于这种愈合。
将牛蛙胃底黏膜的配对两半置于Ussing室中，通过腔内暴露于1 mol/L NaCl 10分钟造成损伤。
已知会干扰内源性bFGF的腔内鱼精蛋白或苏拉明在中性腔内pH值（pHL）下显著抑制电生理恢复。可防止bFGF酸降解的腔内八硫酸蔗糖酯以及一种外源性、耐酸形式的bFGF可在pHL为3.0时实现电生理恢复，而这在对照组织中完全阻止了修复。电生理恢复与形态学修复密切相关。用单克隆抗体进行阳性染色证实了正常和正在修复的牛蛙黏膜中存在内源性bFGF。
得出结论，表面损伤后的快速上皮修复至少部分是由bFGF介导的。
