Department of Medicine, Gastrointestinal Unit, University of Bern, Inselspital, Bern, Switzerland.
Inflammopharmacology. 1997;5(4):407-14. doi: 10.1007/s10787-997-0036-3.
The promotion of the concept of cytoprotection has fostered hopes that the use of co-prescribed mucosal protective agents would revolutionize the prevention of NSAID-induced ulcers and supply the basis for novel ulcer therapy. Prostaglandins do not, however, accelerate ulcer healing when applied at doses that exert an unequivocal cytoprotective activity. Attempts have therefore been made in recent years to create new less-toxic NSAIDs, such as combined lipoxygenase/cyclo-oxygenase inhibitors, NSAIDs coupled to an NO donor and so-called COX-2 inhibitors. All these preparations do in fact exert a diminished gastrointestinal toxicity. There is however increasing evidence accumulating from studies performed in and outside our laboratories that in chromic ulcer models their increased gastrointestinal tolerance is not necessarily reflected by non-interference with ulcer healing. It is thus mandatory to distinguish between cytoprotective and healing properties of drugs interfering with the cyclo-oxygenase pathway.
促进细胞保护概念的发展，使人们希望联合使用黏膜保护剂将彻底改变 NSAID 诱导性溃疡的预防，并为新型溃疡治疗提供基础。然而，当应用于发挥明确细胞保护活性的剂量时，前列腺素并不能加速溃疡愈合。因此，近年来人们试图创造新的毒性较低的 NSAIDs，例如联合脂氧合酶/环加氧酶抑制剂、与 NO 供体偶联的 NSAIDs 和所谓的 COX-2 抑制剂。所有这些制剂实际上确实降低了胃肠道毒性。然而，越来越多的证据来自我们实验室内外的研究表明，在慢性溃疡模型中，它们增加的胃肠道耐受性不一定反映在不干扰溃疡愈合上。因此，必须区分干扰环加氧酶途径的药物的细胞保护和愈合特性。
