Experimental Study On The Changes Of Gut Hormone, Apoptosis Of Epithelial Cells In Gastric Mucosa And Cyclooxygenase During Recovery From Stress Ulceration

ObjectiveThe purposes of this study were to produce the model of stress ulceration with rats exposition to water immersion-restraint stress and to observe the changes of ulcer index, gut hormone, apoptosis of epithelial cells in gastric mucosa. cyclooxygenase(COX) and their interaction during the recovery from the stress ulcer, to investigate the course and the mechanism of gastric mucosa dynamic change events during recovery from stress damage after rats exposed to water immersion -restraint stress(WRS). MethodsWe produce the model of rats with stress ulceration by methods of WRS. And to observe ulcer index and pathology changes during healing course, touse radioimmunoassay to measure serum gastrin and somatostatin ,prostaglandin in gastric mucosa and epidermal growth factor in gastric juice; to detect express changes of COX with imrnunohistochemistry and RT-PCR methods and to observe morphous changes of apoptotic epithelial cells in gastric mucosa and changes of apoptosis index during healing course of rats with stress ulcer using electron microscopy and TUNEL ( Terminaldeoxynucleatidyl transferase mediated DUTP nick and labeling ) techniques.Results1. Produce a model of rats with stress ulceration.2. WRS could induce stress ulceration in gastric mucosa, the damage mucosa improve gradually with the time of healing course.3. Serum gastrin level rose significantly during the recovery from stress ulceration after withdraw from WRS; serum somatostatin level declined significantly; prostaglandin E2 generation in gastric mucosa of Oh group was significantly reduced by( about 50%), prostaglandin E2 generation in gastric mucosa of 0h,2h,4h,6hgroup rose progressively with healing time passing, significant difference compared to control group(P<0.05); prostaglandin E2 generation of 12h and 24h group is close to that of control group, and there aren't remarkable difference between them(P> 0.05 ). measure EGF with a certain amount in the gastric juice, EGF concentrations in gastric juice increased significantly at every corresponding period during the recovery from stress ulcer (P <0.05).The level of gastrin, prostaglandin and EGF were inverse correlation with ulcer index.4. COX-2 expressed in gastric mucosa of control group much low. It is expressed and increased notably during the healing course after termination of WRS; COX-1 expressed in gastric mucosa of control group and each group during the healing course after termination of WRS.5. The electron microscopy showed that morphous of normal mucosa cells in control group are regular, the nucleole type is round in shape, chromatin is even in density; apoptotic changes are manifold such as hetemchro-chromation ,condensation with characteristic crescentic cap appearance, cell shrinkage; seeing nuclear fragmentation and increased vacuoles in intracytoplasm of some apoptotic mucosa cells ,but cellular membrane keep integrity. Few apoptotic mucosa cell could be detected in control group using TUNEL techniques. The apoptotic quantities rose significantly to reach a peak at 6h after the termination of WRS, then thequantities declined but failed to return to the level recorded in the intactmucosa.Conclusion1: WRS could induce gastric mucosa stress ulceration, which appears superficial erosion in line or spot shape. The mucosa damage improves gradually with healing time passing.2: Contents of gastrin, prostaglandin and EGF increase significantly during recovery from stress ulcer, which could protect the damaged mucosa; Contents of somatostatin decline significantly.3: COX-1 and COX-2 expressed in gastric mucosa during recovery from stress ulceration that are beneficial for damaged mucosa, its mechanism is mainly concerned with prostaglandin induced by COX-2 instead of COX-1.4: Apoptotic quantities rose significantly during recovery from stress ulceration, that's beneficial to the damaged mucosa..