86 0

Dexmedetomidine confers neuroprotection against transient global cerebral ischemia/reperfusion injury in rats by inhibiting inflammation through inactivation of the TLR-4/NF-κB pathway

Title
Dexmedetomidine confers neuroprotection against transient global cerebral ischemia/reperfusion injury in rats by inhibiting inflammation through inactivation of the TLR-4/NF-κB pathway
Author
김유진
Keywords
Inflammation; Dexmedetomidine; Neuroprotection; TLR-4; NF-kappa B
Issue Date
2017-05
Publisher
ELSEVIER IRELAND LTD
Citation
NEUROSCIENCE LETTERS, v. 649, page. 20-27
Abstract
Dexmedetomidine (DXM) has anti-inflammatory effects, which is considered an important mechanism of DXM-induced neuroprotection from cerebral ischemia/reperfusion injury. We determined whether the anti-inflammatory effects of DXM are associated with inhibition of the toll-like receptor (TLR)-4/nuclear factor kappa B (NF-kappa B) pathway in a rat model of transient global cerebral ischemia/reperfusion injury. Fifty rats were randomly assigned to one of five groups (10 rats/group): Group S received no treatment; Group C underwent transient global ischemia (10 min); Group D received DXM 30 min before ischemia; Group R received resatorvid, a selective TLR-4 antagonist, 30 min before ischemia; and Group RD received resatorvid and DXM 30 min before ischemia. The numbers of necrotic and apoptotic cells and the levels of TLR-4, NF-kappa B, and caspase-3 were assessed 1 day after ischemia, and pro-inflammatory cytokines including tumor necrosis factor alpha (INF-alpha), interleukin 1 beta (IL-1 beta),and interleukin 6 (IL-6) were measured before ischemia and 2, 6, and 24 h thereafter. The necrotic and apoptotic cell counts and levels of TLR-4, NF-kappa B, and caspase-3 were higher in Group C than in other groups. TNF-alpha were higher in Group C than in other groups 2 h after ischemia, whereas IL-6 were higher in Group C6 h after ischemia. IL-1 beta was higher in Group C than in Group D 6 and 24 h after ischemia. Our findings suggest that the anti-inflammatory action of DXM via inactivation of the TLR-4/NF-kappa B pathway, in part, may explain DXM-induced neuroprotection after cerebral ischemia. (C) 2017 Elsevier B.V. All rights reserved.
URI
https://www.sciencedirect.com/science/article/abs/pii/S0304394017303026?via%3Dihubhttps://repository.hanyang.ac.kr/handle/20.500.11754/114077
ISSN
0304-3940; 1872-7972
DOI
10.1016/j.neulet.2017.04.011
Appears in Collections:
COLLEGE OF MEDICINE[S](의과대학) > MEDICINE(의학과) > 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