Hydroxychloroquine inhibiting neutrophil extracellular trap formation alleviates hepatic ischemia/reperfusion injury by blocking TLR9 in mice

Copyright © 2020 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 216(2020) vom: 01. Juli, Seite 108461
1. Verfasser: Zhang, Sigong (VerfasserIn)
Weitere Verfasser: Zhang, Qiuyue, Wang, Furong, Guo, Xuehui, Liu, Tao, Zhao, Yang, Gu, Baohong, Chen, Hao, Li, Yumin
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2020
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Tlr9 protein, mouse Toll-Like Receptor 9 Hydroxychloroquine 4QWG6N8QKH Protein-Arginine Deiminase Type 4 EC 3.5.3.15 rac GTP-Binding Proteins EC 3.6.5.2
Beschreibung
Zusammenfassung:Copyright © 2020 Elsevier Inc. All rights reserved.
Hepatic ischemia/reperfusion (I/R) injury may arise after partial hepatectomy and liver transplantation. Neutrophil extracellular traps (NETs) were involved in hepatic I/R injury. This study tested the hypothesis that blocking NETs formation could be a potential therapeutic target against hepatic I/R injury. NETs were excessively formed within liver and in serum of I/R mice models and were testified to be an independent contributor to hepatic I/R injury. Hydroxychloroquine (HCQ) alleviated hepatic I/R injury by inhibiting NETs formation in SCID and c57BL/6 mice models. In vitro, HCQ inhibited neutrophils to form NETs at a concentration of 100 μg/ml. CpG-ODN reversed the effect of HCQ inhibiting NETs formation. HCQ inhibited PAD4 and Rac2 expressions by blocking TLR9. NETs are essential contributors to hepatic I/R injury. HCQ blocking TLR9 protects against hepatic I/R injury by inhibiting NETs formation, which may suggest utility of HCQ or other TLR9 agonists for preventing hepatic I/R injury in clinical practices
Beschreibung:Date Completed 01.02.2021
Date Revised 13.12.2023
published: Print-Electronic
ErratumIn: Clin Immunol. 2021 Apr;225:108681. doi: 10.1016/j.clim.2021.108681. - PMID 33548795
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2020.108461