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Tin Protoporphyrin Provides Protection Following Cerebral Hypoxia-Ischemia: Involvement of Alternative Pathways
Citation
Sutherland, BA and Shaw, OM and Clarkson, AN and Winburn, IC and Errington, AC and Dixon, CL and Lees, G and Sammut, IA and Appleton, I, Tin Protoporphyrin Provides Protection Following Cerebral Hypoxia-Ischemia: Involvement of Alternative Pathways, Journal of neuroscience research, 89 pp. 1284-1294. ISSN 0360-4012 (2011) [Refereed Article]
Copyright Statement
Copyright 2011 Wiley-Liss,
Abstract
The contribution of heme oxygenase (HO)-linked pathways
to neurodegeneration following cerebral hypoxiaischemia
(HI) remains unclear. We investigated whether
HO modulators affected HI-induced brain damage and
explored potential mechanisms involved. HI was
induced in 26-day-old male Wistar rats by left common
carotid artery ligation, followed by exposure to a
humidified atmosphere of 8% oxygen for 1 hr. Tin protoporphyrin
(SnPP; an HO inhibitor), ferriprotoporphyrin
(FePP; an HO inducer), or saline was administered intraperitoneally
once daily from 1 day prior to HI until
sacrifice at 3 days post-HI. SnPP reduced (P < 0.05)
infarct volume compared with saline-treated animals,
but FePP had no effect on brain injury. SnPP did not
significantly inhibit HO activity at 3 days post-HI, but
SnPP increased (P < 0.001) total nitric oxide synthase
(NOS) activity compared with HI 1 saline. Both inducible
NOS and cyclooxygenase activities were attenuated
(P < 0.05) by SnPP, whereas mitochondrial complex I
and V activities were augmented (P < 0.05) by SnPP.
SnPP had no effect on NMDA receptor currents. Overall,
like other HO inhibitors, SnPP produced many nonselective
effects, such as attenuation of inflammatory
enzymes and increased mitochondrial respiratory function,
which were associated with a protective response
3 days post-HI.
Item Details
Item Type: | Refereed Article |
---|---|
Keywords: | heme oxygenase, neurorpotection, nitric oxide synthase, cyclooxygenase, mitochondria |
Research Division: | Biomedical and Clinical Sciences |
Research Group: | Neurosciences |
Research Field: | Central nervous system |
Objective Division: | Expanding Knowledge |
Objective Group: | Expanding knowledge |
Objective Field: | Expanding knowledge in the health sciences |
UTAS Author: | Sutherland, BA (Associate Professor Brad Sutherland) |
ID Code: | 113398 |
Year Published: | 2011 |
Web of Science® Times Cited: | 6 |
Deposited By: | Office of the School of Medicine |
Deposited On: | 2016-12-22 |
Last Modified: | 2017-11-06 |
Downloads: | 0 |
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