摘要
急性胰腺炎肺损伤(AP-ALI)是急性胰腺炎临床常见的并发症,炎症性水肿是该病持续进展的关键病理机制之一。水通道蛋白(AQPs)是细胞中水液代谢的基础调控蛋白,其受核因子-κB(NF-κB)、脂氧素A4(LXA4)、丝裂原活化蛋白激酶(MAPK)、环腺苷酸(cAMP)信号通路的调节进而参与AP-ALI炎症性水肿的疾病进展。本文主要描述了AQPs的生理病理机制及其与AP-ALI炎症发生的关系,以期为急性胰腺炎肺损伤的临床治疗提供参考。
Acutepancreatitis-acute lung injury(AP-ALI)is a common clinical complication of acute pancreatitis.Inflammatory edema is one of the key pathological mechanism of the disease progresses.Aquaporin(AQPs)is the basic regulatory protein of water metabolism in cells,which is regulated by nuclear factor-κB(NF-κB),lipoxin A4(LXA4),mitogen-activated protein kinase(MAPK)and cyclic adenosine monophosphate(cAMP)signaling pathways and is involoved in the disease progression of AP-ALI inflammatory edema.This paper mainly describes the physiological and pathological mechanism of AQPs and its relationship with AP-ALI inflammation,in order to provide reference for the clinical treatment of acute pancreatitis lung injury.
作者
赵泓彰
张延英
白敏
文林林
宋冰
王琼
杨润泽
康万荣
李存祥
汪永锋
ZHAO Hong-zhang;ZHANG Yan-ying;BAI Min;WEN Lin-lin;SONG Bing;WANG Qiong;YANG Run-ze;KANG Wan-rong;LI Cun-xiang;WANG Yong-feng(School of Basic Medicine,Gansu University of Traditional Chinese Medicine,Lanzhou 730000,Gansu Province,China;Gansu Experimental Animal Industry Technology Center,Lanzhou 730000,Gansu Province,China)
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2023年第7期1050-1054,共5页
The Chinese Journal of Clinical Pharmacology
基金
国家自然科学基金资助项目(82160871)
甘肃省中医药管理局重点基金资助项目(GZKZ-2021-10)
甘肃省自然科学基金资助项目(20JR5RA186)。
关键词
急性胰腺炎
肺损伤
水通道蛋白
机制
药物开发
acute pancreatitis
lung injury
aquaporin
mechanism
drug development