热盐水致大鼠萎缩性胃炎血清和胃黏膜组织SOD和TAC的变化

Alterations of SOD and TAC in serum and gastric mucosa of atrophic gastritis rat caused by high-salt hot water

目的:观察过热、过咸饮食引起胃黏膜损伤以致造成胃黏膜萎缩的过程中超氧化物歧化酶(SOD)及总抗氧化力(TAC)的动态变化.方法:采用55℃,150 g/L NaC l连续灌胃12 wk,制成大鼠萎缩性胃炎模型,对照组采用等量的25℃水灌胃,在此期间每隔4 wk处死一批大鼠.将大鼠麻醉后腹主动脉取血分离血清,同时摘取胃组织,制成组织匀浆,分别测定血清及胃黏膜组织中SOD和TAC含量.SOD测定采用改良的盐酸羟胺法,TAC采用南京建成生物公司的试剂盒,总蛋白测定采用Lowry s法.结果:与对照组相比较,经热盐水灌饲大鼠的血清和胃黏膜组织中SOD活性及TAC水平显著降低(P<0.05,P<0.05),并且随处理时间延长,SOD活性和TAC降低愈显著.结论:SOD和TAC的显著改变说明活性氧损伤在萎缩性胃炎发生发展过程中起着重要的先导作用,也提示有效的抗氧化干预很可能对于预防萎缩性胃炎具有很好的防治作用.

AIM： To investigate the dynamic variation of superoxide dismutase （SOD） and total antioxidant capacity （TAC） in the process of atrophic gastritis formation caused by over salty hot diet. METHODS： The atrophic gastritis rat model was made by feeding 150 g/L salty water of 55℃ for 12 weeks. The normal control was fed with pure water of 25℃. The rats were killed group by group every 4 weeks and the serum and gastric mucosa were kept to test SOD and TAC. Tissue slice of gastric mucosa was observed under optic microscope. The SOD was tested by improved muriatic acid hydroxylamine method, the total albumen content of stomach homogenate was tested by Lowry＇s method and TAC was tested by TAC kits. RESULTS： In the 12th week, the gastric mucosa in rats fed with high-salt hot water presented with typical pathological change as atrophic gastritis, but this pathological change was absent in control group. SOD and TAC in serum and gastric mucosa had a perfect time-effect relation in hot-salt water group. With the time prolonged, the SOD and TAC decreased significantly in hot-salt water group. CONCLUSION： Active oxygen damnification plays an important precursory role in the formation and evolution of atrophic gastritis.