The role of neutrophil extracellular traps in β-methylamino L-alanine-induced liver injury in mice.

Autor: Ma Y; Department of Health Toxicology, School of Public Health, Dalian Medical University, Dalian 116044, PR China., Tang P; National-Local Joint Engineering Research Center for Drug-Research and Development (R & D) of Neurodegenerative Diseases, Dalian Medical University, Dalian 116044, PR China., Xu J; Department of Health Toxicology, School of Public Health, Dalian Medical University, Dalian 116044, PR China., Li T; Department of Health Toxicology, School of Public Health, Dalian Medical University, Dalian 116044, PR China., Zhang J; Department of Health Toxicology, School of Public Health, Dalian Medical University, Dalian 116044, PR China., Li H; First Affiliated Hospital of Dalian Medical University, Dalian 116044, PR China., Bai Y; First Affiliated Hospital of Dalian Medical University, Dalian 116044, PR China., Wang Q; Department of Anesthesiology, Affiliated Zhongshan Hospital of Dalian University, Dalian 116023, China. Electronic address: wangq1998@aliyun.com., Wang Q; Department of Health Toxicology, School of Public Health, Dalian Medical University, Dalian 116044, PR China; National-Local Joint Engineering Research Center for Drug-Research and Development (R & D) of Neurodegenerative Diseases, Dalian Medical University, Dalian 116044, PR China. Electronic address: wangq4@126.com.
Jazyk: angličtina
Zdroj: Ecotoxicology and environmental safety [Ecotoxicol Environ Saf] 2024 Aug; Vol. 281, pp. 116678. Date of Electronic Publication: 2024 Jul 03.
DOI: 10.1016/j.ecoenv.2024.116678
Abstrakt: The non-protein amino acid β-N-methylamino-L-alanine (BMAA), produced by cyanobacteria, has been recognized as a neurotoxin. L-serine as an antagonist of BMAA can effectively alleviate BMAA-induced neurotoxicity. Although BMAA has long been emphasized as a neurotoxin, with the emergence of BMAA detected in a variety of algae in freshwater around the world and its clear biological enrichment effect, it is particularly important to study the non-neurotoxic adverse effects of BMAA. However, there is only limited evidence to support the ability of BMAA to cause oxidative damage in the liver. The exact molecular mechanism of BMAA-induced liver injury is still unclear. The formation of neutrophil extracellular traps (NETs) is a 'double-edged sword' for the organism, excessive formation of NETs is associated with inflammatory diseases of the liver. Our results innovatively confirmed that BMAA was able to cause the formation of NETs in the liver during the liver injury. The possible mechanism may associated with the regulation of ERK/p38 and cGAS/STING signaling pathways. The massive formation of NETs was able to exacerbate the BMAA-induced oxidative stress and release of inflammatory factors in the mice liver. And the removal of NETs could alleviate this injury. This article will bring a new laboratory evidence for BMAA-induced non-neurotoxicity and immunotoxicity.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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