|本期目录/Table of Contents|

[1]张凌云,赵威.嗜酸细胞浸润食管固有肌层诱导小鼠贲门失弛缓症样食管运动障碍[J].天津医科大学学报,2022,28(06):609-614.
 ZHANG Ling-yun,ZHAO Wei.Eosinophilic infiltration into the muscularis propria of the esophagus induces achalasialike esophageal dyskinesia in mice[J].Journal of Tianjin Medical University,2022,28(06):609-614.
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嗜酸细胞浸润食管固有肌层诱导小鼠贲门失弛缓症样食管运动障碍(PDF)
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
28卷
期数:
2022年06期
页码:
609-614
栏目:
基础医学
出版日期:
2022-11-20

文章信息/Info

Title:
Eosinophilic infiltration into the muscularis propria of the esophagus induces achalasialike esophageal dyskinesia in mice
文章编号:
1006-8147(2022)06-0609-06
作者:
张凌云赵威
天津医科大学总医院消化科,天津300052
Author(s):
ZHANG Ling-yunZHAO Wei
(Department of Gastroenterology and Hepatology,General Hospital,Tianjin Medical University,Tianjin 300052,China)
关键词:
贲门失弛缓症嗜酸性粒细胞神经元
Keywords:
achalasiaeosinophilsneurons
分类号:
R573.7
DOI:
-
文献标志码:
A
摘要:
目的:评估食管固有肌层嗜酸性粒细胞浸润对小鼠食管运动的影响。方法:通过长期卵白蛋白(OVA)刺激建立食管肌层嗜酸性粒细胞浸润小鼠模型。比较模型组(n=30)和对照组(n=20)固有肌层的嗜酸性粒细胞和肌层神经元的数量以及食管运动参数,如食管下括约肌压力(LESP)和食管排空。此外,比较模型组各时间点食管的组织学和运动情况。结果:与对照组相比,模型组食管运动功能严重恶化,与贲门失驰缓(AC)食管运动异常相似,肌层嗜酸性粒细胞增加(t=4.587,P<0.000 1),肌层神经元减少(t=-4.283,P<0.000 1)。随着OVA刺激时间的延长,模型组食管动力障碍加重(第28天时,LESP、食管通过时间、贲门通过时间P<0.05),食管肌层嗜酸性粒细胞增多(第28天时,t=4.429,P=0.000 3),肌间神经元减少(第28天时,t=-4.328,P=0.000 4)。此外,嗜酸性粒细胞浸润与食管肌间神经元数量呈负相关(r=0.531,P=0.026)。结论:长期OVA刺激可引起食管固有肌层嗜酸性粒细胞浸润、肌间神经元减少和食管动力障碍,食管肌层嗜酸性粒细胞浸润可能在 AC 的发病机制中起重要作用。
Abstract:
Objective: To evaluate the effect of eosinophil infiltration in myenteric propria of esophaguson esophageal motility in mice. Methods: A mouse model of eosinophilic infiltration in esophageal muscularis was established by long-term ovalbumin(OVA) stimulation. The numbers of eosinophils and muscularis neurons in the myenteric propria and esophageal motility parameters such as lower esophageal sphincter pressure(LESP) and esophageal emptying were compared between the model group(n=30)and the control groups(n=20). In addition,the histology and motility of the esophagus at each time point in the model group were compared. Results: Compared with the control group,the esophageal motor function of the model group was severely deteriorated,similar to the abnormal esophageal motility of the achalasia(AC),the muscle layer eosinophils increased(t=4.587,P<0.000 1),and the muscle layer neurons decreased(t=-4.283,P<0.000 1). With the prolongation of OVA stimulation time,the esophageal motility disorder aggravated in the model group(on the 28th day,LESP,esophageal transit time,and cardiac transit time,P<0.05),and the eosinophilia in the esophageal muscle layer increased(t=4.429,P=0.000 3 on day 28),myenteric neurons decreased(t=-4.328,P=0.000 4 on day 28). In addition,eosinophil infiltration was negatively correlated with the number of esophageal myenteric neurons(r=0.531,P=0.026). Conclusion: Long-term OVA stimulation can induce eosinophil infiltration in the esophageal muscularis propria,decrease of myenteric neurons and esophageal motility disorders,and eosinophilic infiltration of the esophageal muscularis may play an important role in the pathogenesis of AC.

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备注/Memo

备注/Memo:
基金项目 天津市科委基金(20JCYBJC00450,20JCQNJC00560)
作者简介 张凌云(1993-),女,医师,硕士在读,研究方向:消化系病;
通信作者:赵威,E-mail:wzhao02@tmu.edu.cn。
更新日期/Last Update: 2022-11-20