文献类型：期刊文献

中文题名：治萎防变胶囊对萎缩性胃炎大鼠胃黏膜NO/NOS和胃泌素、内皮素的影响

英文题名：Study on influence of Zhiweifangbian capsule on levels of NO and NOS in gastric tissues,level of gastrin in serum and content of ET-1 in plasma of rats with chronic atrophic gastritis

作者：成映霞[1];段永强[1];朱立鸣[1];张虹[2];程容[1]

第一作者：成映霞

机构：[1]甘肃中医学院基础课部,甘肃兰州730020;[2]甘肃省第二人民医院

第一机构：甘肃中医药大学

年份：2011

卷号：31

期号：4

起止页码：611

中文期刊名：中国老年学杂志

外文期刊名：Chinese Journal of Gerontology

收录：CSTPCD;;北大核心:【北大核心2008】；CSCD:【CSCD2011_2012】；

基金：甘肃省中医管理局科技计划项目(07-GZK-07);甘肃中医学院中青年基金项目(05ZQ-03)

语种：中文

中文关键词：一氧化氮;一氧化氮合酶;胃泌素;内皮素;慢性萎缩性胃炎;治萎防变胶囊

外文关键词：Zhiweifangbian capsule ; Chronic atrophic gastritis ; NO ; Nitric oxide synthase ; Gastrin ; Endothelin-1

摘要：目的探讨治萎防变胶囊对慢性萎缩性胃炎(CAG)大鼠胃黏膜一氧化氮(NO)/一氧化氮合酶(NOS)和血清胃泌素(GAS)、血浆内皮素(ET-1)的影响。方法采用综合法成功复制CAG动物模型。施药治疗后分别对各组大鼠胃黏膜组织NO/NOS及GAS、ET-1含量进行检测。结果与空白组比较,模型组大鼠胃黏膜组织NO/NOS水平显著升高(P<0.01,P<0.05),血清GAS含量显著升高(P<0.05),血浆ET-1含量显著升高(P<0.05);与模型组比较,治萎防变胶囊可显著降低胃黏膜组织NO/NOS和血浆ET-1含量(P<0.05),显著提高血清GAS含量(P<0.05),且以治萎防变胶囊大剂量组作用显著。结论治萎防变胶囊具有提高机体抗氧化能力,减轻自由基损伤;降低血浆ET-1含量,促进血清GAS分泌,增加胃动力,改善胃黏膜血流量的作用。
Objective To study effects of Zhiweifangbian capsule （ZWFB） on levels of NO and NOS in gastric tissues, level of gastrin in serum and content of ET-1 in plasma of rats with chronic atrophic gastritis （CAG）. Methods CAG model of was established with synthetic method. The levels of NO and NOS in gastric tissues, level of gastrin in serum and content of ET-1 in plasma were detected. Results In model group, levels of NO and NOS in gastric tissues and content of ET-1 in plasma were much higher than those of normal group （ P 〈 0. 01, P 〈 0. 05 ）, level of gastrin in serum was much lower than that of normal group （ P 〈 0. 05 ）. Compared with model group, ZWFB could decrease content of NO and NOS in gastric tissues and ET-1 in plasma, increase level of gastrin in serum significantly （ all P 〈 0. 05）. Conclusions ZWFB has functions of ameliorating gastric mucosal blood flow and microcirculation, elevating antioxidation enzyme activity, lessening free radical impairment and restraining lipid peroxidation.