Int. J. Mol. Sci. 2010, 11(2), 544-561; https://doi.org/10.3390/ijms11020544
Novel Neuroprotective Strategies in Ischemic Retinal Lesions
1
Department of Experimental Zoology and Neurobiology, University of Pecs, H-7624 Pecs, Hungary
2
Department of Biochemistry and Medical Chemistry, University of Pecs, H-7624 Pecs, Hungary
3
Department of Anatomy, University of Pecs, H-7624 Pecs, Hungary
4
Department of Sportbiology, University of Pecs, H-7624 Pecs, Hungary
*
Author to whom correspondence should be addressed.
Received: 7 January 2010 / Revised: 27 January 2010 / Accepted: 27 January 2010 / Published: 3 February 2010
(This article belongs to the Special Issue Neuroprotective Strategies (special issue))
Abstract
Retinal ischemia can be effectively modeled by permanent bilateral common carotid artery occlusion, which leads to chronic hypoperfusion-induced degeneration in the entire rat retina. The complex pathways leading to retinal cell death offer a complex approach of neuroprotective strategies. In the present review we summarize recent findings with different neuroprotective candidate molecules. We describe the protective effects of intravitreal treatment with: (i) urocortin 2; (ii) a mitochondrial ATP-sensitive K+ channel opener, diazoxide; (iii) a neurotrophic factor, pituitary adenylate cyclase activating polypeptide; and (iv) a novel poly(ADP-ribose) polymerase inhibitor (HO3089). The retinoprotective effects are demonstrated with morphological description and effects on apoptotic pathways using molecular biological techniques. View Full-TextKeywords:
BCCAO; ischemia; retinoprotection; urocortin 2; diazoxide; PACAP; PARP-inhibitor; rat retina
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This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).
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Szabadfi, K.; Mester, L.; Reglodi, D.; Kiss, P.; Babai, N.; Racz, B.; Kovacs, K.; Szabo, A.; Tamas, A.; Gabriel, R.; Atlasz, T. Novel Neuroprotective Strategies in Ischemic Retinal Lesions. Int. J. Mol. Sci. 2010, 11, 544-561.
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