| Various severe physical and emotional distress are closely related to the formation of acute upper gastrointestional ulcerations with extensive of hemorrhagic lesions. In contrast to previous conceptions that necrosis induced gastric mucosal lesion under stress condition, recent study found apoptosis played an impotent role in the development of stress ulcer. In contrast to necrosis-induced cell death, the apoptosis is considered to be a physiological process leading to cell death, which is active and depends on RNA and proteins synthesis by the dying cell, and elimination of the dying cells without involvement of an inf]ammatoiy response. It bad been identified the preservation of gastric mucosal integrity is a complex biological process involving the balance between epithelial cell proliferation and programmed cell death tenned apoptosis, and several pro- and anti- apoptotic factors such as Bcl-2/Ba~?Fas/FasL system were involved in the regulation of apoptosis, however, the way and the precise mechanism of gastric mucosa cell death under stress conditions are still unknown. Cell to cell communication is impoitant in controlling cell growth, specific genes expression and differentiation, which is also important for cells responding to varies stress, both NO as a messenger or modulator among cells, which has been shown to modulate cell apoptosis at different condition and 0(43 -the specialized cell adhesion system in tissues for intercellular communication maybe play important roles for gastric cell population dynamics (apoptosis, niitosis) under stress condition. The effects of antiulcer agents with different phaimacodynamics on this process is also unknown. The purpose of this study was to investigate the course and the mechanism of gastric mucosa dynamic change events during and after rats exposed to water immersion-restraint stress. 1. Induction of stress lesion Water immersion-restraint stress model were performed with the way 7 Brodie DA described previously. The extent gastiic mucosal lesion was evaluated grossly and histologically at WRS2h,3.5h and 2h,5h,8h,l2h~24h alter termination of WRS. The results revealed that comparing with intact gastric mucosa of rats in non-exposed to WRS, several spotted haemorrhagic lesion were detected in the oxyntic gandular area at 2h exposed to WRS, some patchy exfoliation of surface epithelial cells was microscopically observecL Exposure to WRS for 3.5h to 2h alter WRS result in an appearance ofmultiple gastric lesion in the ox~tic mucosaAvficroscopical examination of mucosa after 3.5h of WRS revealed wide spread damage of the surface epithelium with numerous cells sloughed oft the ulceration appeared in the gastric mucosa as craters, almost extending to the muscularis mucosae, mucosa and submucosa were apparently congestive and edematous, which was significantly reduced already at 5h alter WRS and then finther significantly declined at 12h and almost disappear at 24 h after the withdrawal fl~m WRS. The results suggested that WRS could induce gastiic mucosa lesion successfully, the mucosa change under stress was a dynamic process, in which the mucosa lesion would be severer and severer with time passing under stress conditions and gradually reduced until the stiucture of the gastric mucosa returning to normal after the withdrawal fonn WRS. 2~ Measurement of cell death and proliferation of gastric epithelial...
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