Eastwood G L
School of Medicine, Medical College of Georgia, Augusta 30912.
J Clin Gastroenterol. 1991;13 Suppl 1:S48-53. doi: 10.1097/00004836-199112001-00008.
The constant, rapid renewal of the gastroduodenal epithelium is an important mechanism of mucosal protection because it maintains the functional integrity of the epithelium. It also is necessary for the repair of mucosal injury. Aspirin, indomethacin, and ethanol all have been shown to stimulate epithelial proliferation in the experimental setting. The stimulatory effects of these agents may be a compensatory reaction to mild injury and may contribute to the process of mucosal adaptation. On the other hand, corticosteroids, physiologic stress, and smoking appear to depress epithelial proliferation, which could render the mucosa susceptible to the effects of other ulcerogens as well as retard the healing of existing mucosal lesions. Epithelial proliferation in mucosa adjacent to active duodenal ulcers as well as from nonulcerated duodenitis is increased when compared to normal-appearing mucosa. This stimulation of epithelial proliferation may be caused by inflammation; it is not known whether ulcer patients have a defect in epithelial proliferation that precedes ulceration. Although prostaglandins (PGs) protect ulceration. Although prostaglandins (PGs) protect the gastroduodenal mucosa, the weight of evidence indicates that PGs do not have a primary effect on epithelial proliferation but rather retard senescence and loss of epithelial cells. The result is thickening of the mucosa, which may contribute to the protective effects of PGs. Ulcerogenic agents or conditions may either depress epithelial proliferation, which predisposes to ulceration or the ulcerogenic effects of other ulcerogens, or result in a hyperproliferative response, which may contribute to the process of mucosal adaptation and protection.
胃十二指肠上皮的持续快速更新是黏膜保护的重要机制，因为它维持上皮的功能完整性。这对于黏膜损伤的修复也很必要。阿司匹林、吲哚美辛和乙醇在实验环境中均已显示能刺激上皮增殖。这些药物的刺激作用可能是对轻度损伤的一种代偿反应，可能有助于黏膜适应过程。另一方面，皮质类固醇、生理应激和吸烟似乎会抑制上皮增殖，这可能使黏膜易受其他致溃疡因素的影响，并延缓现有黏膜损伤的愈合。与外观正常的黏膜相比，活动性十二指肠溃疡附近以及非溃疡性十二指肠炎的黏膜上皮增殖增加。这种上皮增殖的刺激可能由炎症引起；尚不清楚溃疡患者在溃疡形成之前是否存在上皮增殖缺陷。虽然前列腺素（PGs）可保护胃十二指肠黏膜，但大量证据表明，PGs对上皮增殖没有主要作用，而是延缓上皮细胞的衰老和丢失。结果是黏膜增厚，这可能有助于PGs的保护作用。致溃疡因素或状况可能会抑制上皮增殖，从而易引发溃疡或其他致溃疡因素的致溃疡作用，或者导致增殖过度反应，这可能有助于黏膜适应和保护过程。
