Impairment and Regeneration of Gastric Mucosa After Irradiation in Mice.

OBJECTIVE: To understand the effects of γ-ray irradiation (IR) on the proliferation of gastric mucosal cells and to investigate the possible mechanisms that affect gastric mucosal cell proliferation. STUDY DESIGN: C57BL/6J mice were exposed to IR at various doses (4, 8, and 15 Gy). We measured the changes of gastric mucosal BrdU-positive cells and the expression of ß-catenin protein in the isthmus of fundic glands at days 1, 3, and 5 after irradiation. RESULTS: Our data showed that the mice that received 15 Gy IR died within 4 days. IR caused gastric mucosal injury in mice, and the degree of injury increased along with the increasing doses. Compared with the control group, the proliferation of gastric mucosal cells was inhibited 1 day after irradiation. Cell proliferation was recovered on day 5 after low-dose (4 and 8 Gy) IR, while proliferation was continuously inhibited after high-dose (15 Gy) IR. ß-catenin expression was increased and had a translocation in the isthmus of gastric mucosa. CONCLUSION: These findings suggest that gastric mucosa is sensitive to irradiation. The Wnt/ß-catenin pathway is activated and plays a role in cell proliferation of gastric mucosa upon irradiation.

Observation of microvasculature in intestinal wall after burn in rats.

OBJECTIVE: To investigate the relationship between intestinal mucosa injury and changes in stereologic parameters for its vessels. STUDY DESIGN: PAS stain was used to observe the basement membrane of intestinal epithelium. To measure the parameters of microvasculature by stereology, microvasculature was shown by alkaline phosphatase stain. Diamine oxidase (DAO) activity was determined by spectrophotometry. RESULTS: Red mucus became thinner than that of the control group; basement membrane was disrupted at 3 post burn hours (PBH). Changes became more serious at 6 and 12 PBH. Villus height and crypt depth appeared shortened at post burn. Microvasculature diameter was reduced. Mean section area at 12 PBH was significantly lower than that of the control group (p < 0.01). Mean circumference at 6 PBH was 19.43 +/- 1.59 microm and in the control group 23.84 +/- 4.17 microm. After burn injury, DAO activity in the intestine was reduced, falling to minimum at 12 PBH (p < 0.01), and in plasma was raised significantly, reaching peak at 12 PBH (p < 0.05). CONCLUSION: Our results suggest disruption of basement membrane, reduction of microvasculature diameter and DAO activity in intestine will appear at post burn, which induces decreased blood flow in intestine and damage to intestinal mucosa.