急性胰腺炎肝损伤的分子机制  

Molecular mechanism of liver injury in acute pancreatitis

作　　者：徐文倩 郭敏[2] 王晓[2] 吴瑶麒 张近远 李合国[2] XU Wenqian;GUO Min;WANG Xiao;WU Yaoqi;ZHANG Jinyuan;LI Heguo(The First Clinical Medical College of Henan University of Chinese Medicine,Zhengzhou 450000,China;Department of Hepatology and Spleen-Stomach,The First Affiliated Hospital of Henan University of Chinese Medicine,Zhengzhou 450000,China)

机构地区：[1]河南中医药大学第一临床医学院,郑州450000 [2]河南中医药大学第一附属医院脾胃肝胆科,郑州450000

出　　处：《临床肝胆病杂志》2022年第11期2663-2668,共6页Journal of Clinical Hepatology

基　　金：河南省特色骨干学科中医学学科建设项目(STG-ZYX02-202116);河南省中医药科学研究重大专项课题(2018ZYZD06);国家自然科学基金(81904161)。

摘　　要：急性胰腺炎进展十分迅速,如不及时控制,可能引发多脏器损伤,更有甚者会因器官功能衰竭而死亡。目前因肝衰竭而死亡的急性胰腺炎患者比例仍较大。肝脏与胰腺在生理上相互联系,在病理上相互影响。本文通过胰腺与肝脏的生理联系、细胞因子、炎症反应、氧化应激、微循环障碍及肠道菌群移位等6个方面对急性胰腺炎肝损伤的分子机制进行阐述。Acute pancreatitis often progresses rapidly,and if it is not controlled in time,it may lead to multiple organ injury and even death due to organ failure.At present,there is still a high proportion of patients with acute pancreatitis who died due to liver failure.The liver and the pancreas are interrelated physiologically and affect each other pathologically.This article elaborates on the molecular mechanism of liver injury in acute pancreatitis from the six aspects of the physiological relationship between the pancreas and the liver,cytokines,inflammatory response,oxidative stress,microcirculation disturbance,and intestinal flora translocation.

关 键 词：急性胰腺炎 肝损伤 细胞因子类 

分 类 号：R576[医药卫生—消化系统] R575[医药卫生—内科学]