Apoptosis in the gastric mucosa: molecular mechanisms, basic and clinical implications.

摘要: Apoptosis a programmed cell death, is an essential mechanism of eliminating damaged or aged cells and thus to maintain tissue integrity. There are two central pathways that lead apoptosis: a) the positive induction by ligands (death factors) binding plasma membrane receptors factor receptors) b) negative loss suppressor activity. The common execution mechanisms apoptosis consist activation cytosolic aspartate-specific proteases (ICE-proteases) termed caspases, which can be activated via various intracellular pathways. In stomach, mucosal surface epithelial constantly exfoliating gastric lumen completely replaced within 3-5 days under physiological conditions. has been reported take place in all regions stomach with apoptotic occurring predominantly superficial parts glands, at rate 2-3% for cells. Following injury (e.g. ulcer development), rapidly increases remains elevated 2-3 months. 3-month old scar, mucous, parietal, chief endocrine was found similar normal mucosa. Helicobacter pylori (H. pylori) infection induces mucosa this action appears independent VacA cytotoxin H. strains. Nonsteroidal anti-inflammatory drugs (NSAIDs), especially cyclooxygenase-2 (COX-2) inhibitors potent inductors apoptosis. However, they abrogate proliferation effects induced pylori. Many details exact molecular regulating remain elucidated.