氧化应激、NOD样受体蛋白3炎症小体及细胞焦亡在食管炎性损伤中的研究进展

Research progress of oxidative stress, NLRP-3 inflammasome and pyroptosis in esophageal inflammatory injury

食管炎性损伤常由胃和十二指肠内容物逆行流入食管,诱发不适症状和食管黏膜病理病变。胃食管反流病(GERD)是一种由反复酸/胆汁酸刺激的食管慢性炎症性疾病可能会通过氧化损伤途径增加患癌症的风险。胃灼热和反流是GERD的典型症状,非典型表现的数量估计超过100种,包括非心脏性胸痛、支气管肺或耳鼻喉症状以及牙齿侵蚀。对这种化生转化发生的细胞和分子机制的理解仍然有限。GERD诱导食管组织活性氧氧化应激积累和慢性炎症局部浸润反应,炎症小体在该反应中发挥重要调控作用。细胞焦亡广泛参与消化系统各个脏器疾病的发生、发展,进一步阐述其在胃肠道疾病中的发生机制具有重要意义。本文主要综述了国内外氧化应激、NOD样受体蛋白3炎性小体以及细胞焦亡在食管氧化损伤和炎症发生发展中的机制研究现况作一综述,为其进一步临床诊疗及机制探索提供一定理论依据。

Inflammatory injury of the esophagus often results from retrograde flow of contents from the stomach and duodenum into the esophagus,inducing discomfort symptoms and pathological changes in the esophageal mucosa.Gastroesophageal reflux disease(GERD)is a chronic inflammatory disease of the esophagus that is stimulated by repeated acid/bile acids,which may increase the risk of cancer through oxidative damage pathways.Gastric burning and reflux are typical symptoms of GERD,with an estimated number of over 100 atypical manifestations,including non cardiac chest pain,bronchopulmonary or otolaryngological symptoms,and tooth erosion.The understanding of the cellular and molecular mechanisms underlying this transformation is still limited.GERD induces the accumulation of reactive oxygen species oxidative stress in esophageal tissue and chronic inflammatory local infiltration response,in which inflammasomes play an important regulatory role.Pyroptosis is widely involved in the occurrence and development of digestive system diseases.This article mainly reviews the current research status of the mechanism of oxidative stress,NOD like receptor protein inflammasome and pyroptosis in the occurrence and development of esophageal oxidative damage and inflammation at home and abroad,providing a theoretical basis for its further clinical diagnosis and treatment and mechanism exploration.