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中华胃食管反流病电子杂志

中华胃食管反流病电子杂志 ›› 2022, Vol. 09 ›› Issue (04) : 209 -214. doi: 10.3877/cma.j.issn.2095-8765.2022.04.008

综述

胃食管反流病与NLRP-3炎症小体相关性研究进展
玉苏普·艾麦尔1, 买买提·依斯热依力2, 克力木·阿不都热依木3,†()   
  1. 1. 830001 乌鲁木齐，新疆维吾尔自治区人民医院微创、疝和腹壁外科；830001 乌鲁木齐，新疆医科大学
    2. 830001 乌鲁木齐，新疆维吾尔自治区人民医院微创、疝和腹壁外科；830001 乌鲁木齐，新疆维吾尔自治区普外微创研究所；830001 乌鲁木齐，新疆维吾尔自治区人民医院胃食管反流病及减重代谢外科临床研究中心
    3. 830001 乌鲁木齐，新疆维吾尔自治区人民医院微创、疝和腹壁外科；830001 乌鲁木齐，新疆维吾尔自治区普外微创研究所；830001 乌鲁木齐，新疆医科大学；830001 乌鲁木齐，新疆维吾尔自治区人民医院胃食管反流病及减重代谢外科临床研究中心
  • 收稿日期:2022-04-19 出版日期:2022-11-15
  • 通信作者: 克力木·阿不都热依木
  • 基金资助:
    新疆维吾尔自治区自然科学基金(2021D01C148); 新疆维吾尔自治区自然科学基金(2022D01C107)

The relationship between GERD and NLRP-3 inflammasome

Aimaier Yusupu1, MaimaitiYisireyili2, Kelimu·Abudureyimu3,†()   

  1. 1. Department of Minimally Invasive Surgery, Hernia and Abdominal Wall Surgery, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830001, China; Graduate School of Xinjiang Medical University, Urumqi 830001, China
    2. Department of Minimally Invasive Surgery, Hernia and Abdominal Wall Surgery, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830001, China; Research Institute of General and Minimally Invasive Surgery, Xinjiang Uygur Autonomous Region, Urumqi 830001, China; Xinjiang Uygur Autonomous Region Gastroesophageal Reflux Disease and Weight Loss Metabolism Surgery Clinical Research Center, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830001, China
    3. Department of Minimally Invasive Surgery, Hernia and Abdominal Wall Surgery, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830001, China; Research Institute of General and Minimally Invasive Surgery, Xinjiang Uygur Autonomous Region, Urumqi 830001, China; Graduate School of Xinjiang Medical University, Urumqi 830001, China; Xinjiang Uygur Autonomous Region Gastroesophageal Reflux Disease and Weight Loss Metabolism Surgery Clinical Research Center, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830001, China
  • Received:2022-04-19 Published:2022-11-15
  • Corresponding author: Kelimu·Abudureyimu
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玉苏普·艾麦尔, 买买提·依斯热依力, 克力木·阿不都热依木. 胃食管反流病与NLRP-3炎症小体相关性研究进展[J]. 中华胃食管反流病电子杂志, 2022, 09(04): 209-214.

Aimaier Yusupu, MaimaitiYisireyili, Kelimu·Abudureyimu. The relationship between GERD and NLRP-3 inflammasome[J]. Chinese Journal of Gastroesophageal Reflux Disease(Electronic Edition), 2022, 09(04): 209-214.

胃食管反流病（GERD）是当胃内容物反流到食管引起症状和/或并发症时发生的一系列疾病。炎症小体在炎症相关疾病的发生发展机制中发挥重要作用，而其中核苷酸结合寡化结构域样受体-3（NLRP-3）炎症小体是当前研究最为深入的炎症小体，其他家族成员包括NLRP-1、NAIP以及NLRC4等。NLRP-3炎症小体能够被多种病原相关分子模式和损伤相关分子模式激活，进而活化caspase-1，释放成熟形式的白细胞介素-1β（IL-1β）和IL-18，引起机体的炎症反应并参与多种疾病的发生发展。近年来，炎症因子在GERD发病机制的研究成为新的研究热点，已有相关研究证实NLRP-3炎症小体在多种疾病过程中都发挥了关键作用。本文结合国内外文献对NLRP-3炎症小体与胃食管反流间的关系及其可能机制进行综述。

关键词: 胃食管反流病, 炎症因子, 核苷酸结合寡化结构域样受体-3

Gastroesophageal reflux disease (GERD) is a series of diseases that occur when the reflux of gastric contents to the esophagus causes symptoms and/or complications. Inflammatory corpuscles play an important role in the occurrence and development of inflammation related diseases. Among them, nucleotide binding oligodomain like receptor-3 (NLRP-3) inflammatory corpuscles are the most deeply studied inflammatory corpuscles. Other family members include nlrp-1, NAIP and nlrc4. NLRP-3 inflammasome can be activated by a variety of pathogen associated molecular patterns (PAM PS) and damage associated molecular patterns (damps), and then activate caspase-1 and release mature forms of interleukin-1β (IL-1β) And IL-18, which cause the body's inflammatory response and participate in the occurrence and development of a variety of diseases. In recent years, the study of inflammatory factors in the pathogenesis of GERD has become a new research hotspot. Relevant studies have confirmed that nlrp-3 inflammatory bodies play a key role in a variety of diseases. Combined with the literature at home and abroad, this paper reviews the relationship between nlrp-3 inflammatory bodies and gastroesophageal reflux and its possible mechanism.

Key words: Gastroesophageal reflux disease, Inflammatory factors, Nucleo tide-binding oligodomain-like receptor-3
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