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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.

Varga B, Gesztelyi R, Bombicz M, Haines D, Szabo AM, Kemeny-Beke A, Antal M, Vecsernyes M, Juhasz B, Tosaki A - J. Mol. Neurosci. (2013)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Faculty of Pharmacy, Medical and Health Science Center, University of Debrecen, Nagyerdei krt. 98, Debrecen, 4032, Hungary. varga.balazs@pharm.unideb.hu

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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Electroretinograms (group I-a) of baseline (a) and ischemic/reperfused (b) eyes of vehicle-treated (control) animals and ischemic/reperfused eyes of rats treated with 50, 250, 500, and 1,000 μg/kg α-MSH (c–f, respectively)
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Fig1: Electroretinograms (group I-a) of baseline (a) and ischemic/reperfused (b) eyes of vehicle-treated (control) animals and ischemic/reperfused eyes of rats treated with 50, 250, 500, and 1,000 μg/kg α-MSH (c–f, respectively)

Mentions: The initial objective of work performed in part I of the present study was to identify an effective dose range of α-MSH using ERG. Figure 1 shows actual voltage levels and the time course of ERG spikes observed in part I studies, while percentages of mean values of all ischemic b waves relative to control baseline are shown in Fig. 2. Significant differences between non-I/R values were not observed (data not shown).Fig. 1


Protective effect of alpha-melanocyte-stimulating hormone (α-MSH) on the recovery of ischemia/reperfusion (I/R)-induced retinal damage in a rat model.

Varga B, Gesztelyi R, Bombicz M, Haines D, Szabo AM, Kemeny-Beke A, Antal M, Vecsernyes M, Juhasz B, Tosaki A - J. Mol. Neurosci. (2013)

Electroretinograms (group I-a) of baseline (a) and ischemic/reperfused (b) eyes of vehicle-treated (control) animals and ischemic/reperfused eyes of rats treated with 50, 250, 500, and 1,000 μg/kg α-MSH (c–f, respectively)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3675276&req=5

Fig1: Electroretinograms (group I-a) of baseline (a) and ischemic/reperfused (b) eyes of vehicle-treated (control) animals and ischemic/reperfused eyes of rats treated with 50, 250, 500, and 1,000 μg/kg α-MSH (c–f, respectively)
Mentions: The initial objective of work performed in part I of the present study was to identify an effective dose range of α-MSH using ERG. Figure 1 shows actual voltage levels and the time course of ERG spikes observed in part I studies, while percentages of mean values of all ischemic b waves relative to control baseline are shown in Fig. 2. Significant differences between non-I/R values were not observed (data not shown).Fig. 1

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Faculty of Pharmacy, Medical and Health Science Center, University of Debrecen, Nagyerdei krt. 98, Debrecen, 4032, Hungary. varga.balazs@pharm.unideb.hu

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.

Show MeSH
Related in: MedlinePlus