血红素氧合酶-1/一氧化碳系统对脓毒症肺损伤时细胞器调控作用的研究进展  

Research advances of the regulation of heme oxygenase-1/carbon monoxide system on organelles during sepsis-induced acute lung injury

作　　者：史佳[1,2] 余剑波[1,2] Shi Jia;Yu Jianbo(Department of Anesthesiology,Nankai Clinical College of Tianjin Medical University(Tianjin Nankai Hospital),Tianjin 300100,China;Department of Critical Care Medicine,Nankai Clinical College of Tianjin Medical University(Tianjin Nankai Hospital),Tianjin 300100,China)

机构地区：[1]天津医科大学南开临床学院(天津市南开医院)麻醉科,天津300100 [2]天津医科大学南开临床学院(天津市南开医院)重症医学科,天津300100

出　　处：《国际麻醉学与复苏杂志》2022年第9期988-992,共5页International Journal of Anesthesiology and Resuscitation

基　　金：国家自然科学基金(82004076,81772106);天津市卫生健康委员会科技项目青年项目(QN20027)。

摘　　要：脓毒症急性肺损伤(acute lung injury,ALI)发病急骤,是临床常见的急危重症。研究表明,线粒体动力学、内质网应激(endoplasmic reticulum stress,ERs)、高尔基体应激、溶酶体介导细胞自噬、外泌体分泌转移等细胞器功能障碍在脓毒症ALI发生发展的病理生理过程中发挥重要作用。血红素氧合酶-1(heme oxygenase-1,HO-1)及其催化产物一氧化碳(carbon monoxide,CO)是应激状态下细胞重要的内源性保护机制之一,通过发挥抗氧化应激、抗炎、抗凋亡等作用以减轻脓毒症ALI。文章主要阐述HO-1/CO系统对脓毒症ALI时细胞内各重要细胞器如线粒体、内质网、高尔基体、溶酶体、外泌体等的调控作用,为脓毒症ALI基于发病机制的治疗提供新途径和理论依据。Sepsis-induced acute lung injury(ALI)is a rapid onset,typical clinical intensive emergency.Studies have shown that mitochondrial dynamics,endoplasmic reticulum stress(ERs),Golgi apparatus stress,lysosome-mediated autophagy,exosome secretion and transfer play an essential role in the pathophysiological process of septic ALI.Heme oxygenase-1(HO-1)and its catalytic byproducts,carbon monoxide(CO),are one of the crucial endogenous protective mechanisms of cells under stress,which can alleviate septic ALI through antioxidant,anti-inflammatory,and anti-apoptosis effects.This review mainly elaborates the role of HO-1/CO system in regulating the intracellular key organelles such as mitochondria,endoplasmic reticulum,golgi apparatus,lysosome,exosome in the settings of septic ALI,which provides a new approach and theoretical basis for the prevention and treatment of septic ALI.

关 键 词：脓毒症 急性肺损伤 细胞器 血红素氧合酶-1 一氧化碳 

分 类 号：R459.7[医药卫生—急诊医学]