• 1. Department of Gastrointestinal Surgery/Hernia and Abdominal Wall Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, R. P. China;
  • 2. Experiment Center of Shandong University of Traditional Chinese Medicine, Jinan 250355, R. P. China;
  • 3. Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, R. P. China;
LI Zhitong, Email: jylizhitong@163.com
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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)-1β 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.

Citation: LI Zhitong, KONG Xianglin, LIU Bingrong, LIU Dan, WANG Meng, LI Deliang. Preliminary verification of animal model of benign esophageal stricture caused by gastroesophageal reflux in rats. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2024, 31(6): 690-694. doi: 10.7507/1007-9424.202309076 Copy

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