Reducing Effect of IL-32 alpha in the Development of Stroke Through Blocking of NF-kappa B, but Enhancement of STAT3 Pathways

Title
Reducing Effect of IL-32 alpha in the Development of Stroke Through Blocking of NF-kappa B, but Enhancement of STAT3 Pathways
Author(s)
최동영황철주[황철주]윤형문[윤형문]정유연[정유연]이동훈[이동훈]윤나영[윤나영]서현옥[서현옥]한진이[한진이]오기완[오기완]한상배[한상배]윤도영[윤도영]홍진태[홍진태]
Keywords
CEREBRAL-ARTERY OCCLUSION; ISCHEMIA-REPERFUSION INJURY; PERMANENT FOCAL ISCHEMIA; PROTECTS RAT BRAINS; OXIDATIVE STRESS; NEURODEGENERATIVE DISORDERS; ALZHEIMERS-DISEASE; SIGNAL TRANSDUCER; OXYGEN RADICALS; TRANSCRIPTION 3
Issue Date
201504
Publisher
HUMANA PRESS INC
Citation
MOLECULAR NEUROBIOLOGY, v.51, no.2, pp.648 - 660
Abstract
Neuroinflammation is important for the development of several neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and stroke. Since changes of cytokine level are critical for neuroinflammation in the brain, we investigated whether IL-32 alpha overexpression could change neuroinflammation and, thus, affect stroke development. Middle cerebral artery occlusion (MCAO) induced development of ischemia, and ischemic neuronal cell death were reduced in IL-32 alpha-overexpressing transgenic mice (IL-32 alpha mice) brain through the decreased release of neuroinflammatory cytokines (IL-6, IL-1 beta, TNF-alpha) and activation of astrocytes, but enhancement of anti-neuroinflammatory cytokines (IL-10). Reactive oxygen species generation and lipid peroxidation as well as expression of inducible nitric oxide and cyclooxygenase-2 were also reduced in the IL-32 alpha mice brain. Nuclear factor-kappa B (NF-kappa B), a critical transcriptional factor regulating neuroinflammation, was much lower, but activation of signal transducer and activator of transcription 3 (STAT3), which plays a crucial role in cell survival and proliferation, was much higher in IL-32 alpha-overexpressing mice brain compared to those of wild-type mice brain. These results suggest that IL-32 alpha can prevent cerebral ischemia damage via upregulation of anti-neuroinflammatory cytokine expression and STAT3 activation, but downregulation of neuroinflammatory cytokines and NF-kappa B activation.
URI
http://hdl.handle.net/YU.REPOSITORY/32816http://dx.doi.org/10.1007/s12035-014-8739-0
ISSN
0893-7648
Appears in Collections:
약학대학 > 약학부 > Articles
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE