Sevoflurane post-conditioning increases nuclear factor erythroid 2-related factor and haemoxygenase-1 expression via protein kinase C pathway in a rat model of transient global cerebral ischaemia.
- Authors
- Kim, Eu gene; Park, Y. H.; Jeon, Y. T.; Hwang, J. W.; Lim, Y. J.; Kim, E.; Park, S. Y.; Park, H. P.
- Issue Date
- Feb-2015
- Publisher
- OXFORD UNIV PRESS
- Keywords
- anaesthetics, inhalation; GA-binding protein transcription factor; haeme oxygenase-1; protein kinase C
- Citation
- BRITISH JOURNAL OF ANAESTHESIA, v.114, no.2, pp.307 - 318
- Indexed
- SCIE
SCOPUS
- Journal Title
- BRITISH JOURNAL OF ANAESTHESIA
- Volume
- 114
- Number
- 2
- Start Page
- 307
- End Page
- 318
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/157888
- DOI
- 10.1093/bja/aeu268
- ISSN
- 0007-0912
- Abstract
- Background. The antioxidant mechanism of sevoflurane post-conditioning-induced neuroprotection remains unclear. We determined whether sevoflurane post-conditioning induces nuclear factor erythroid 2-related factor (Nrf2, a master transcription factor regulating antioxidant defence genes) and haemoxygenase-1 (HO-1, an antioxidant enzyme) expression, and whether protein kinase C (PKC) is involved in Nrf2 activation, in a rat model of transient global cerebral ischaemia/reperfusion (I/R) injury.
Methods. Eighty-six rats were assigned to five groups: sham (n=6), control (n=20), sevoflurane post-conditioning (two cycles with 2 vol% sevoflurane inhalation for 10 min, n=20), chelerythrine (a PKC inhibitor; 5 mg kg(-1) i.v. administration, n=20), and sevoflurane post-conditioning plus chelerythrine (n=20). The levels of nuclear Nrf2 and cytoplasmic HO-1 were assessed 1 or 7 days after ischaemia (n=10 each, apart from the sham group, n=3).
Results. On day 1 but not day 7 post-ischaemia, Nrf2 and HO-1 expression were significantly higher in the sevoflurane post-conditioning group than in the control group. Chelerythrine administration reduced the elevated Nrf2 and HO-1 expression induced by sevoflurane post-conditioning.
Conclusions. Sevoflurane post-conditioning increased Nrf2/HO-1 expression via PKC signalling in the early phase after transient global cerebral I/R injury, suggesting that activation of antioxidant enzymes may be responsible for sevoflurane post-conditioning-induced neuroprotection in the early phase after cerebral I/R injury.
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