Matúz J
Pharmacological Research Centre, Chemical Works of Gedeon Richter Ltd., Budapest, Hungary.
Acta Physiol Hung. 1992;80(1-4):189-94.
Gastrointestinal mucus is considered an important part of the mucosal defence mechanism against endogenous aggressors such as acid and pepsin. The mucus gel layer, adherent to the mucosal surface creates a diffusion barrier to luminal pepsin, thus protecting the underlying epithelium from the digestion by pepsin. The mucolytic pepsin will, however, digest the mucus at its luminal surface, but that lost is normally balanced by secretion of new mucus. This dynamic balance is disrupted when the mucus is exposed to excess pepsin, which causes focal haemorrhagic damage by progressively hydrolyzing the adherent mucus. The adherent mucus gel layer cannot contribute to the protection against exogen damaging agents such as ethanol and nonsteroidal anti-inflammatory drugs, as these compounds easily penetrate the mucus barrier causing, at high concentration, epithelial exfoliation. This study describes the basic properties and characteristics of gastric mucus and compares the pepsin-induced damage with the ethanol damage model.
胃肠道黏液被认为是黏膜防御机制对抗内源性侵害者(如胃酸和胃蛋白酶)的重要组成部分。附着于黏膜表面的黏液凝胶层对腔内胃蛋白酶形成扩散屏障,从而保护下层上皮细胞免受胃蛋白酶的消化。然而,具有黏液溶解作用的胃蛋白酶会在其腔面消化黏液,但通常新黏液的分泌会平衡这种损失。当黏液暴露于过量胃蛋白酶时,这种动态平衡就会被打破,过量胃蛋白酶会通过逐渐水解附着的黏液导致局部出血性损伤。附着的黏液凝胶层无法抵御外源性损伤剂,如乙醇和非甾体抗炎药,因为这些化合物很容易穿透黏液屏障,在高浓度时会导致上皮细胞脱落。本研究描述了胃黏液的基本特性,并比较了胃蛋白酶诱导的损伤与乙醇损伤模型。