胃食管反流致大鼠食管良性狭窄动物模型的初步验证
Preliminary verification of animal model of benign esophageal stricture caused by gastroesophageal reflux in rats
李治仝 1孔祥琳 2刘冰熔 3刘丹 3王盟 3李德亮3
作者信息
- 1. 郑州大学第一附属医院胃肠外科/疝和腹壁外科(郑州 450052)
- 2. 山东中医药大学实验中心(济南 250355)
- 3. 郑州大学第一附属医院消化内科(济南 450052)
- 折叠
摘要
目的 建立胃食管反流致食管狭窄的大鼠模型,探讨食管狭窄形成的机制.方法 30只雄性SD大鼠采用随机数字表法随机均分为3组:手术+酸灌注组,先制作食管下括约肌松弛和食管裂孔疝模型,然后用盐酸.胃蛋白酶灌注大鼠食管;酸灌注组,直接用盐酸-胃蛋白酶灌注大鼠食管;对照组,用生理盐水灌注大鼠食管.连续灌注4周后,观察3组SD大鼠食管黏膜损伤情况,并采用酶联免疫吸附测定法检测食管组织中相关的炎性细胞因子[肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素(interleukin,IL)-1β和IL-18]的浓度.结果 在手术+酸灌注组中,有2只SD大鼠出现食管狭窄,而酸灌注组和对照组未发现食管狭窄.手术+酸灌注组和酸灌注组大鼠的体质量低于对照组(P＜0.05).大鼠的食管黏膜损伤评分手术+酸灌注组和酸灌注组高于对照组(P＜0.001),手术+酸灌注组又高于酸灌注组(P=0.014).食管组织中的TNF-α、IL-1β和IL-18浓度手术+酸灌注组和酸灌注组高于对照组(P＜0.001),手术+酸灌注组又高于酸灌注组(P＜0.001).结论 抗反流屏障是防止胃食管反流病的重要组成部分.抗反流屏障破坏、盐酸-胃蛋白酶灌注和炎性细胞因子共同诱导食管炎症和损伤,甚至造成食管狭窄的发生.
Abstract
Objective To develop an experimental model of gastroesophageal reflux-induced esophageal stricture in rats and explore the mechanism of esophageal stricture.Methods A total of 30 male Sprague-Dawley(SD)rats by random number table method were randomly divided into three groups as follows:an operation+acid perfusion group,first the models of lower esophageal sphincter relaxation and hiatal hernia were made,and then the rats'esophagus were perfused with hydrochloric acid-pepsin;acid perfusion group,the rats'esophagus were directly perfused with hydrochloric acid-pepsin;and control group,rats'esophagus were perfused with normal saline.After 4 weeks of continuous perfusion,the esophageal mucosal injury of SD rats in each group were observed,and the concentrations of inflammatory cytokines[tumor necrosis factor-α(TNF-α),interleukin(IL)-1 β and IL-18]in esophageal tissues were detected by enzyme-linked immunosorbent assay.Results In the operation+acid perfusion group,esophageal stricture was formed in 2 SD rats,but no esophageal stenosis was found in the acid perfusion group and the control group.The body weight of rats in the operation+acid perfusion group and the acid perfusion group were lower than that in the control group(P＜0.05).The esophageal mucosal injury scores of rats in the operation+acid perfusion group and the acid perfusion group were higher than that in the control group(P＜0.001),and the operation+acid perfusion group was higher than that in the acid perfusion group(P=0.014).The concentrations of TNF-α,IL-1β and IL-18 in esophageal tissues were higher in the operation+acid perfusion group and the acid perfusion group than that in the control group(P＜0.001),and the operation+acid perfusion group was higher than that in the acid perfusion group(P＜0.001).Conclusions The anti-reflux barrier is an important part of preventing gastroesophageal reflux disease.The destruction of anti-reflux barrier,hydrochloric acid-pepsin perfusion and inflammatory cytokines jointly induced esophageal inflammation and injury,and even caused esophageal stricture.
关键词
胃食管反流/食管狭窄/盐酸-胃蛋白酶/动物实验Key words
gastroesophageal reflux/esophageal stricture/hydrochloric acid-pepsin/animal experimentation引用本文复制引用
基金项目
河南省医学科技攻关计划省部共建重点项目(SBGJ202102144)
出版年
2024
NETL
NSTL
万方数据