Argon Inhalation Attenuates Retinal Apoptosis After Ischemia/reperfusion Injury in a Time- and Dose-dependent Manner in Rats

Argon Inhalation Attenuates Retinal Apoptosis After Ischemia/reperfusion Injury in a Time- and Dose-dependent Manner in Rats

Auteur : Felix Ulbrich, Nils Schallner, Mark Coburn, Torsten Loop, Wolf A. Lagrèze, Julia Biermann, Ulrich Göbel

Date de publication : 2014

Éditeur : Universität

Nombre de pages : Non disponible

Résumé du livre

Abstract: Purpose:Retinal ischemia and reperfusion injuries (IRI) permanently affect neuronal tissue and function by apoptosis and inflammation due to the limited regenerative potential of neurons. Recently, evidence emerged that the noble gas Argon exerts protective properties, while lacking any detrimental or adverse effects. We hypothesized that Argon inhalation after IRI would exert antiapoptotic effects in the retina, thereby protecting retinal ganglion cells (RGC) of the rat's eye. Methods: IRI was performed on the left eyes of rats (n = 8) with or without inhaled Argon postconditioning (25, 50 and 75 Vol%) for 1 hour immediately or delayed after ischemia (i.e. 1.5 and 3 hours). Retinal tissue was harvested after 24 hours to analyze mRNA and protein expression of Bcl-2, Bax and Caspase-3, NF-k B. Densities of fluorogold-prelabeled RGCs were analyzed 7 days after injury in whole-mounts. Histological tissue samples were prepared for immunohistochemistry and blood was analyzed regarding systemic effects of Argon or IRI. Statistics were performed using One-Way ANOVA.Results:IRI induced RGC loss was reduced by Argon 75 Vol% inhalation and was dose-dependently attenuated by lower concentrations, or by delayed Argon inhalation (1504+-300 vs. 2761+-257; p

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