Dexmedetomidine confers neuroprotection against transient global cerebral ischemia/reperfusion injury in rats by inhibiting inflammation through inactivation of the TLR-4/NF-kappa B pathway
- Authors
- Kim, Eugene; Kim, Hyun-Chang; Lee, Seungmi; Ryu, Ho-Geol; Park, Yong-Hee; Kim, Jun Hyun; Lim, Young-Jin; Park, Hee-Pyoung
- Issue Date
- May-2017
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- Inflammation; Dexmedetomidine; Neuroprotection; TLR-4; NF-kappa B
- Citation
- NEUROSCIENCE LETTERS, v.649, pp 20 - 27
- Pages
- 8
- Journal Title
- NEUROSCIENCE LETTERS
- Volume
- 649
- Start Page
- 20
- End Page
- 27
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/4451
- DOI
- 10.1016/j.neulet.2017.04.011
- ISSN
- 0304-3940
1872-7972
- 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.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - College of Medicine > College of Medicine > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/4451)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.