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      Protective Effect of Alpha-Melanocyte-Stimulating Hormone (α-MSH) on the Recovery of Ischemia/Reperfusion (I/R)-Induced Retinal Damage in A Rat Model

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          Abstract

          The present study demonstrates capacity of α-MSH to augment recovery from ischemia/reperfusion (I/R)-induced retinal damage in vivo and correlation of its protective effects with expression of heme oxygenase-1 (HO-1). Used techniques include ocular ischemia and reperfusion, electroretinography, histology, electron microscopy, and molecular-biological techniques. The results demonstrate the α-MSH-mediated inhibition of I/R-induced functional deterioration of the retina. Outcomes suggest that the protective effects of α-MSH occur mainly through HO-1-dependent pathways but HO-1-independent mechanisms may also contribute to protection. The observation that post-ischemic treatment with α-MSH exhibits therapeutic efficacy in the same range as pre-ischemic treatment, is a novel result. This outcome suggests a highly conserved protective role for α-MSH as a major stress response mechanism—and offers the possibility for development of novel therapeutic strategies utilizing this hormone, in particular in treatment of conditions resulting from I/R injury, such as deterioration of retinal microcirculation. The merit of the study lies in the fact that I/R injury contribute significantly to the severity of retinopathies. However, currently there are no evidence-based treatments for retinal I/R injury available for clinical use. Our finding suggests that α-MSH may have a very wide range of uses in the prevention of I/R-mediated pathologies.

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          Most cited references28

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          The enzymatic conversion of heme to bilirubin by microsomal heme oxygenase.

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            Microvascular lesions of diabetic retinopathy: clues towards understanding pathogenesis?

            Retinopathy is a major complication of diabetes mellitus and this condition remains a leading cause of blindness in the working population of developed countries. As diabetic retinopathy progresses a range of neuroglial and microvascular abnormalities develop although it remains unclear how these pathologies relate to each other and their net contribution to retinal damage. From a haemodynamic perspective, evidence suggests that there is an early reduction in retinal perfusion before the onset of diabetic retinopathy followed by a gradual increase in blood flow as the complication progresses. The functional reduction in retinal blood flow observed during early diabetic retinopathy may be additive or synergistic to pro-inflammatory changes, leucostasis and vaso-occlusion and thus be intimately linked to the progressive ischaemic hypoxia and increased blood flow associated with later stages of the disease. In the current review a unifying framework is presented that explains how arteriolar dysfunction and haemodynamic changes may contribute to late stage microvascular pathology and vision loss in human diabetic retinopathy.
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              Is Open Access

              Current concepts in the pathophysiology of glaucoma

              Glaucoma, the second leading cause of blindness, is characterized by changes in the optic disc and visual field defects. The elevated intraocular pressure was considered the prime factor responsible for the glaucomatous optic neuropathy involving death of retinal ganglion cells and their axons. Extensive investigations into the pathophysiology of glaucoma now reveal the role of multiple factors in the development of retinal ganglion cell death. A better understanding of the pathophysiological mechanisms involved in the onset and progression of glaucomatous optic neuropathy is crucial in the development of better therapeutic options. This review is an effort to summarize the current concepts in the pathophysiology of glaucoma so that newer therapeutic targets can be recognized. The literature available in the National Medical Library and online Pubmed search engine was used for literature review.
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                Author and article information

                Contributors
                varga.balazs@pharm.unideb.hu
                gesztelyi.rudolf@pharm.unideb.hu
                bombicz.mariann@pharm.unideb.hu
                ddhaines2002@yahoo.com
                szadrica@freemail.hu
                kemenyba@med.unideb.hu
                antal@anat.med.unideb.hu
                vecsernyes.miklos@pharm.unideb.hu
                juhasz.bela@pharm.unideb.hu
                +36-52-255586 , +36-52-255586 , tosaki.arpad@pharm.unideb.hu
                Journal
                J Mol Neurosci
                J. Mol. Neurosci
                Journal of Molecular Neuroscience
                Humana Press Inc (New York )
                0895-8696
                1559-1166
                17 March 2013
                17 March 2013
                July 2013
                : 50
                : 3
                : 558-570
                Affiliations
                [ ]Department of Pharmacology, Faculty of Pharmacy, Medical and Health Science Center, University of Debrecen, Nagyerdei krt. 98, Debrecen, 4032 Hungary
                [ ]3rd Department of Internal Medicine, University of Debrecen, Debrecen, Hungary
                [ ]Department of Ophthalmology, University of Debrecen, Debrecen, Hungary
                [ ]Department of Anatomy, University of Debrecen, Debrecen, Hungary
                [ ]Department of Pharmaceutical Technology, University of Debrecen, Debrecen, Hungary
                Article
                9998
                10.1007/s12031-013-9998-3
                3675276
                23504281
                a49bb0fc-ca50-46bd-b4b3-b73432567a86
                © The Author(s) 2013

                Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

                History
                : 18 January 2013
                : 6 March 2013
                Categories
                Article
                Custom metadata
                © Springer Science+Business Media New York 2013

                Neurosciences
                alpha-melanocyte-stimulating hormone,ischemia/reperfusion,retina,electroretinography,heme oxygenase,rat

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