Caffeic acid-vanadium nanozymes treat skin flap ischemia-reperfusion injury through macrophage reprogramming and the upregulation of X-linked inhibitors of apoptotic proteins  

作　　者：Xinyu Zhao Jie Shan Hanying Qian Xu Jin Yiwei Sun Jianghao Xing Qingrong Li Xu-Lin Chen Xianwen Wang 

机构地区：[1]Department of Burns,The First Affiliated Hospital of Anhui Medical University,Hefei 230022,China [2]Department of Graduate School,Anhui University of Chinese Medicine,Hefei 230022,China [3]School of Biomedical Engineering,Anhui Medical University,Hefei 230032,China

出　　处：《Acta Pharmaceutica Sinica B》2025年第1期592-610,共19页药学学报(英文版)

基　　金：supported by the National Natural Science Foundation of China(Grant Nos.82172204,82372552 and 82372517);the Anhui Key Research and Development Plan(Grant No.202104j07020027,China);the Excellent Youth of Natural Science Research Projects in Anhui Province Universities(2023AH030060);the Basic and Clinical Cooperative Research and Promotion Program of Anhui Medical University(No.2021xkjT028,China);the Research Fund of Anhui Institute of Translational Medicine(2022zhyx-C01,China);the Scientific Research Programme for Higher Education Institutions in Anhui Province(2023AH040371,China).

摘　　要：Ischemia-reperfusion(I/R)injury following skin flap transplantation is a critical factor leading to flap necrosis and transplant failure.Antagonizing inflammatory responses and oxidative stress are regarded as crucial targets for mitigating reperfusion injury and enhancing flap survival.In this study,caffeic acid-vanadium metal polyphenol nanoparticles(CA-V NPs)were prepared for the treatment of skin flap ischemia and reperfusion.This study was conducted using a one-step method to prepare new types of CA-V NPs with uniform sizes and stable structures.In vitro,the CA-V NPs exhibited CATlike and SOD-like activities and could effectively scavenge ROS,generate oxygen,and alleviate oxidative stress.In the H_(2)O_(2)-induced cellular oxidative stress model,CA-V NPs effectively reduced ROS levels and inhibited apoptosis through the XIAP/Caspase-3 pathway.In the cellular inflammation model induced by LPS combined with IFN-g,CA-V NPs reprogrammed macrophage polarization toward the M2 phenotype and reduced inflammatory responses by reducing the expression of the chemokines CCL4 and CXCL2.In addition,animal experiments have shown that CA-V NPs can alleviate oxidative stress in skin flap tissues,inhibit apoptosis,promote angiogenesis,and ultimately improve the survival rate of skin flaps.CA-V NPs provide a new target and strategy for the treatment of flap I/R injury。

关 键 词：Caffeic acid-vanadium Nanozymes Skin flap ISCHEMIA-REPERFUSION Oxidative stress Inflammation CHEMOKINES Apoptosis 

分 类 号：R73[医药卫生—肿瘤]