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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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Western blot analysis for HO-1 protein expression (group I-b). The HO-1 content of I/R-injured bulbi is represented in arbitrary units with SEM in animals not receiving α-MSH (control) and rats treated with 500 μg/kg α-MSH. *p < 0.05
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Fig5: Western blot analysis for HO-1 protein expression (group I-b). The HO-1 content of I/R-injured bulbi is represented in arbitrary units with SEM in animals not receiving α-MSH (control) and rats treated with 500 μg/kg α-MSH. *p < 0.05

Mentions: Western blot analysis of HO-1 expression in ocular tissue revealed significantly greater amounts of HO-1 protein in I/R-injured bulbi taken from animals receiving 500 μg/kg α-MSH treatment than from vehicle-treated rats (p < 0.05). The results of these experiments are shown in Fig. 5. Significant differences between control and treated non-I/R values were not observed (data not shown).Fig. 5


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)

Western blot analysis for HO-1 protein expression (group I-b). The HO-1 content of I/R-injured bulbi is represented in arbitrary units with SEM in animals not receiving α-MSH (control) and rats treated with 500 μg/kg α-MSH. *p < 0.05
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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

Fig5: Western blot analysis for HO-1 protein expression (group I-b). The HO-1 content of I/R-injured bulbi is represented in arbitrary units with SEM in animals not receiving α-MSH (control) and rats treated with 500 μg/kg α-MSH. *p < 0.05
Mentions: Western blot analysis of HO-1 expression in ocular tissue revealed significantly greater amounts of HO-1 protein in I/R-injured bulbi taken from animals receiving 500 μg/kg α-MSH treatment than from vehicle-treated rats (p < 0.05). The results of these experiments are shown in Fig. 5. Significant differences between control and treated non-I/R values were not observed (data not shown).Fig. 5

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