Role and mechanisms of cytokines in the secondary brain injury after intracerebral hemorrhage. (July 2019)

• Record Type: Journal Article
• Authors: Zhu, Huimin; Wang, Zhiqiang; Yu, Jixu; Yang, Xiuli; He, Feng; Liu, Zhenchuan; Che, Fengyuan; Chen, Xuemei; Ren, Honglei; Hong, Michael; Wang, Jian
• Is Part Of: Progress in neurobiology. Volume 178(2019)
• Publication Date: 2019-07
• Subjects: Act1 NF-κB activator 1 -- Akt protein kinase B -- AMPA α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid -- AR adenosine receptor -- ATG5 autophagy related 5 -- B7-H1 B7 homolog 1 -- BBB blood–brain barrier -- Bcl-2 B-cell lymphoma 2 -- C/EBPs CCAAT/enhancer binding proteins -- CAA cerebral amyloid angiopathy -- CC-3 cleaved caspase-3 -- CCL2 chemokine (C-C motif) ligand 2 -- CCR2 C-C chemokine receptor type 2 -- CNS central nervous system -- CO carbon monoxide -- CSF cerebrospinal fluid -- CXCL10 C-X-C motif chemokine 10 -- CXCR CXC chemokine receptor -- DAMP damage-associated molecular pattern -- EAE experimental autoimmune encephalomyelitis -- ERK extracellular related kinase -- EV extracellular vesicle -- GCS Glasgow Coma Scale -- GSK3β glycogen synthase kinase 3β -- Hb hemoglobin -- HMGB high mobility group box -- HO heme oxygenase -- HPA axis hypothalamo-pituitary-adrenal axis -- ICAM-1 intercellular adhesion molecule 1 -- ICH intracerebral hemorrhage -- IFN-γ interferon γ -- IL interleukin -- IL-12R IL-12 receptor -- IL-17R IL-17 receptor -- IL-1R IL-1 receptor -- IL-33R IL-33 receptor -- IL-4I1 IL-4 induced one -- IRF7 interferon regulatory factor 7 -- LC3-II light chain 3-II -- MAC membrane attack complex -- MAPK mitogen-activated protein kinase -- MLKL mixed lineage kinase domain-like protein -- MMP matrix metalloproteinase -- MS multiple sclerosis -- MyD88 myeloid differentiation primary response 88 -- NADPH nicotinamide adenine dinucleotide phosphate -- NECA nonselective AR agonist 1-(6-amino-9H-purin-9-yl)-1-deoxy-N-ethyl-b-D-ribofuranuronamide -- NF-κB nuclear factor kappa-light-chain-enhancer of activated B cells -- NK cell natural killer cell -- NLRP3 nucleotide-binding domain and leucine-rich repeat containing protein 3 -- Nrf2 nuclear factor erythroid 2-related factor 2 -- PAMP pathogen-associated molecular pattern -- PAR protease-activated receptor -- pDNA plasmid DNA -- PLGA poly (lactic-co-glycolic-acid) -- PPARγ peroxisome proliferator-activated receptor γ -- PTEN phosphatase and tensin homolog -- RAGE, receptor of advanced glycosylation end product -- RIP receptor interacting protein -- ROS reactive oxygen species -- SEFIR SEF/IL-17R -- SNS sympathetic nervous system -- SOCS suppressor of cytokine signaling -- ST2 suppression of tumorigenicity 2 -- TCR T cell receptor -- TGF-β transforming growth factor-β -- Th cell T helper cell -- TLR Toll-like receptor -- TNF-α tumor necrosis factor-α -- TNF-R tumor necrosis factor receptor -- TRIF TIR-domain-containing adapter-inducing interferon-β -- VCAM-1 vascular cell adhesion molecule 1; ICH -- Secondary injury -- Inflammatory reaction -- Cytokines; Neurobiology -- Periodicals; Neurology -- Periodicals; Neurology -- Periodicals; Neurobiologie -- Périodiques; 612.8
• DOI: 10.1016/j.pneurobio.2019.03.003
• Languages: English
• ISSNs: 0301-0082

Abstract

Abstract: Intracerebral hemorrhage (ICH) is a common and severe cerebrovascular disease that has high mortality. Few survivors achieve self-care. Currently, patients receive only symptomatic treatment for ICH and benefit poorly from this regimen. Inflammatory cytokines are important participants in secondary injury after ICH. Increases in proinflammatory cytokines may aggravate the tissue injury, whereas increases in anti-inflammatory cytokines might be protective in the ICH brain. Inflammatory cytokines have been studied as therapeutic targets in a variety of acute and chronic brain diseases; however, studies on ICH are limited. This review summarizes the roles and functions of various pro- and anti-inflammatory cytokines in secondary brain injury after ICH and discusses pathogenic mechanisms and emerging therapeutic strategies and directions for treatment of ICH.