Mucosal apoptosis induced by ischemia-reperfusion and fasting in the stomach compared to the small intestine in rats

We previously reported that apoptosis was induced in rats intestinal mucosa following long term fasting and ischemia-reperfusion. It is well known that a role of apoptosis in gastric mucosa is important in pathophysiological conditions such as Helicobacter pylori infection. The aim of the present experiment was to examine an effect of ischemia-reperfusion and fasting on apoptosis of gastric mucosa comparing to small intestinal mucosa. Method: Male SD rats(280 330g) were used in the experiments. Under halothane anesthesia, the celiac artery was occluded to induce ischemia in the stomach and the superior mesentric artery was occluded to induce intestinal ischemia. Sixty minutes reperfusion was followed after 60min ischemia. After ischemia-reperfusion, rats were sacrificed and ratios of fragmented DNA to total DNA, agarose gel electrophoresis, and immunohistochemical staining were examined. Additional rats were fasted for 48h before sacrificed to evaluate mucosal apoptosis. Results: The percentage of fragmented DNA after ischemia-reperfusion was significantly increase in the intestinal mucosa(20.7~2.1%) compared to the value in sham treated controls(5.7~1.0%). THe increase in intestinal apoptosis was observed in 48h fasted rats(29.8~4.4%). Agarose gel electrophoresis showed that DNA ladders in both conditions in the intestinal mucosa, indicating that a part of the intestinal mucosal cells were dead by apoptosis. Apoptotic cells in the intestinal mucosa were observed in the immunohistochemical staining. In contrast to the small intestine, the percentage of fragmented DNA after ischemia-reperfusion did not increased in the gastric mucosa after ischcrnia-rcperfusiontz.B'r U.S'a». Induction of apoptosis in the gastric mucosa was not observed following 48h fasting(1.4~0.2%). Neither significant increase in apoptotic cells in the immunohistochemical staining nor DNA ladders in agarose gel electrophoresis was observed in the gastric mucosa in either condition. Conclusion: The results of the present study indicated that induction of apoptosis in the rat gastric mucosa by ischemiareperfusion and fasting was less sensitive compared to the rat intestinal mucosa. The significance of the difference in the sensitivity for apoptosis is not clear, but this discrepancy might explain the difference an incidence of malignant disease and a turn-over ratio in these two organs.