@entity4185 attenuates retinal apoptosis after XXXX /reperfusion injury in a time- and dose-dependent manner in @entity35 .

@entity32 @entity1976 @entity63 @entity2479 @entity2310 @entity4185 @entity35 @entity4124 @entity4026 @entity491 @entity16853
PURPOSE: @entity2479 and reperfusion injuries (IRI) permanently affect neuronal tissue and function by apoptosis and @entity32 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 @entity4185 after IRI would exert antiapoptotic effects in the retina, thereby protecting retinal ganglion cells (RGC) of the @entity35 's eye. METHODS: IRI was performed on the left eyes of @entity35 (n=8) with or without inhaled Argon postconditioning (25, 50 and 75 Vol%) for 1 hour immediately or delayed after @entity63 (i.e. 1.5 and 3 hours). Retinal tissue was harvested after 24 hours to analyze mRNA and protein expression of @entity1976 , @entity2310 and @entity4124 , @entity4026 . Densities of @entity16853 -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 @entity4185 (1504  300 vs. 2761  257; p<0.001). Moreover, Argon inhibited @entity2310 and @entity1976 mRNA expression significantly ( @entity2310 : 1.64  0.30 vs. 0.78  0.29 and @entity1976 : 2.07  0.29 vs. 0.99  0.22; both p<0.01), as well as @entity4124 cleavage (1.91  0.46 vs. 1.05  0.36; p<0.001). Expression of @entity4026 was attenuated significantly. Immunohistochemistry revealed an affection of M  ller cells and astrocytes. In addition, IRI induced @entity491 was reduced significantly after @entity4185 at 75 Vol%. CONCLUSION: Immediate and delayed Argon postconditioning protects IRI induced apoptotic loss of RGC in a time- and dose-dependent manner, possibly mediated by the inhibition of @entity4026 . Further studies need to evaluate Argon's possible role as a therapeutic option.
