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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一氧化氮(NO)及一氧化氮合酶(NOS)的动态变化。以及在该过程中采用抗氧化荆干预胃组织和血清中氧化损伤重要指标丙二醛(MDA)的动态变化。方法采用55℃、1．5％NaCl 对实验大鼠连续灌胃每日1次,对照组采用等量的25℃水灌胃。在灌胃期间每隔4周处死一批大鼠。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,分别采用试剂盒测定血清和胃组织中NO和NOS。采用Lowry’s法测定组织匀浆中总蛋白的含量。结果实验动物血清中NO和NOS活性随着大鼠周龄的增加而升高,以热盐水组升高显著。胃黏膜组织中NO和NOS活性随着时间的延长逐渐升高,而12周后,随着时间的延长,表现出了下降的趋势。结论提示热盐水所致萎缩性胃炎的发病过程中NO在其中发挥着重要作用。
Objective To observe the dynamic changes of nitric oxide (NO) and nitric oxide synthase (NOS) during gastric mucosal atrophy caused by gastric mucosal injury induced by overheating and salty diet. In the process, antioxidant enzymes were used to prevent the dynamic changes of malondialdehyde (MDA), an important indicator of oxidative damage in gastric tissue and serum. Methods The experimental rats were given gavage once a day by 55 ℃ and 1.5% NaCl, while the control group were treated by the same amount of water at 25 ℃. Rats were sacrificed every 4 weeks during gavage. After the rats were anesthetized, the abdominal aorta blood was taken to separate the serum and the gastric tissues were harvested at the same time to make tissue homogenates. The contents of NO and NOS in serum and stomach tissue were determined by kit respectively. Lowry’s method was used to determine the total protein content in the tissue homogenate. Results The NO and NOS activity in the serum of experimental animals increased with the increase of the age of the rats and markedly increased with the heat saline group. The activity of NO and NOS in gastric mucosa gradually increased with time, but decreased with the time after 12 weeks. Conclusions suggest that NO plays an important role in the pathogenesis of atrophic gastritis caused by hot salt water.