文献类型：期刊文献

中文题名：香砂六君子汤对慢性萎缩性胃炎大鼠胃黏膜相关因子水平的影响

英文题名：Effects of Xiangsha Liujunzi Decoction on Levels of Gastric Mucosa-related Factors of Chronic Atrophic Gastritis Rats

作者：白敏[1];成映霞[1];段永强[1,2];王丽园[1,3];杨晓轶[1];巩子汉[1];马骏[1]

第一作者：白敏

机构：[1]甘肃中医药大学,甘肃兰州730000;[2]甘肃省中医方药挖掘与创新转化重点实验室,甘肃兰州730000;[3]苍溪县中医医院,四川苍溪628400

第一机构：甘肃中医药大学

年份：2020

卷号：27

期号：11

起止页码：52

中文期刊名：中国中医药信息杂志

外文期刊名：Chinese Journal of Information on Traditional Chinese Medicine

收录：CSTPCD;;CSCD:【CSCD_E2019_2020】；

基金：国家自然科学基金(81260519、81760830)。

语种：中文

中文关键词：香砂六君子汤;慢性萎缩性胃炎;一氧化氮;诱导型一氧化氮合酶;内皮型一氧化氮合酶;P选择素;白细胞内皮细胞黏附分子-1;内皮素-1;大鼠

外文关键词：Xiangsha Liujunzi Decoction;chronic atrophic gastritis;NO;iNOS;eNOS;SELP;LECAM-1;ET-1;rats

摘要：目的观察香砂六君子汤对慢性萎缩性胃炎(CAG)大鼠胃黏膜诱导型一氧化氮合酶(iNOS)、内皮型一氧化氮合酶(eNOS)表达及下游一氧化氮(NO)、P选择素(SELP)、白细胞内皮细胞黏附分子-1(LECAM-1)、内皮素-1(ET-1)含量的影响,探讨其治疗CAG的分子机制。方法将SPF级健康Wistar大鼠120只随机分为空白组和造模组,造模组大鼠采用综合法(MNNG+雷尼替丁+饥饱失常法)复制CAG模型,成模后按随机数字表法将其分为模型组、维酶素组和香砂六君子汤高、中、低剂量组。模型组和空白组每日给予2 mL蒸馏水灌胃,香砂六君子汤高、中、低剂量组分别给予24、12、6 g/(kg?d)香砂六君子汤药液灌胃,维酶素组给予0.3 g/(kg?d)维酶素连续灌胃,连续120 d。观察大鼠一般生存状况和胃黏膜病理学变化,采用RT-qPCR、Western blot分别检测CAG大鼠胃黏膜组织iNOS、eNOS基因和蛋白的表达,采用ELISA检测大鼠胃黏膜组织NO、SELP、LECAM-1、ET-1含量。结果与空白组比较,模型组大鼠一般生存状况相对较差,胃黏膜变薄,固有层腺体减少,腺体疏松、排列不规则,散在大量炎性细胞浸润,iNOS基因和蛋白表达显著升高,eNOS基因和蛋白表达显著降低,胃黏膜组织NO、SELP、LECAM-1、ET-1含量显著升高,差异均有统计学意义(P<0.05);与模型组比较,香砂六君子汤高、中、低剂量组和维酶素组大鼠一般生存状况不同程度改善,胃黏膜仍较薄,固有层腺体增多,炎性细胞浸润减轻,胃黏膜组织eNOS基因和蛋白表达显著升高,iNOS基因和蛋白表达显著降低,NO、SELP、LECAM-1、ET-1含量显著降低,其中香砂六君子汤高剂量组差异有统计学意义(P<0.05)。结论香砂六君子汤可能通过下调CAG大鼠胃黏膜组织iNOS表达、上调eNOS表达,达到抑制下游因子NO、SELP、LECAM-1、ET-1分泌,进而调节CAG大鼠胃黏膜炎性微环境的稳态,发挥保护胃黏膜作用。
Objective To investigate the effects of Xiangsha Liujunzi Decoction on the expressions of iNOS and eNOS in gastric mucosa and the contents of SELP,LECAM-1 and ET-1 in the downstream of chronic atrophic gastritis(CAG)rats;To explore the molecular mechanism of its treatment of CAG.Methods Totally 120 healthy Wistar rats of SPF grade were randomly divided into blank group and CAG model group.CAG model rats were made by MNNG+ranitidine+anorexia method.According to random number table method,they were divided into model group,vitacoenzyme group and Xiangsha Liujunzi Decoction high-,medium-,low-dosage groups.Model group and blank group were given 2 mL distilled water;Xiangsha Liujunzi Decoction groups were given 24,12,6 g/(kg?d)Xiangsha Liujunzi Decoction respectively;vitacoenzyme group was given 0.3 g/(kg?d)vitacoenzyme,continuous administration for 120 days.The changes of general living conditions and pathological changes of gastric mucosa in each group were observed.The expression of iNOS,eNOS gene and protein in gastric mucosa were detected by real-time fluorescent quantitative PCR and Western blot.The contents of NO,SELP,LECAM-1 and ET-1 in gastric mucosa were detected by ELISA.Results Compared with the blank group,the rats in the model group had a relatively poorer living condition,thinner gastric mucosa,fewer glands in the lamina propria,loose glands,irregular arrangement,scattered inflammatory cell infiltration,significant increase of iNOS gene and protein expression,significant decrease of eNOS gene and protein expression,and significant increase of NO,SELP,LECAM-1 and ET-1 contents in gastric mucosa,with statistical significance(P<0.05).Compared with the model group,the general living conditions of the rats in Xiangsha Liujunzi Decoction groups and vitacoenzyme group were improved in varying degrees.The gastric mucosa was still thin;the glands in the lamina propria increased;the inflammatory infiltration was reduced;the expression of eNOS gene and protein in the gastric mucosa significantly increased;the expression of iNOS gene and protein was significantly reduced;the contents of NO,SELP,LECAM-1 and ET-1 in the gastric mucosa were reduced;Xiangsha Liujunzi Decoction high-dosage group was significant,with statistical significance(P<0.05).Conclusion Xiangsha Liujunzi Decoction may down-regulate the expression level of iNOS and up-regulate the expression level of eNOS in gastric mucosa of CAG model rats,so as to inhibit the secretion of downstream factors of NO,SELP,LECAM-1 and ET-1,and then regulate the homeostasis of inflammatory microenvironment of gastric mucosa of CAG model rats to play a role in protecting gastric mucosa.