Fig. 4From: The Carbon monoxide releasing molecule ALF-186 mediates anti-inflammatory and neuroprotective effects via the soluble guanylate cyclase ß1 in rats’ retinal ganglion cells after ischemia and reperfusion injuryEffect of ALF-186 treatment on transcription factors NF-κB and CREB. a Fold induction of NF-κB mRNA expression after ALF-186 and sGC inhibition in ischemic retinal tissue compared to GAPDH in relation to the corresponding non-ischemic retinae analyzed by RT-PCR (n = 8; data are mean ± SD; IRI vs. IRI + ALF-186, *** = p < 0.001 and IRI + ALF-186 vs. IRI + ODQ + ALF-186, * = p < 0.05). b Fold induction of CREB mRNA expression in ischemic retinal tissue compared to GAPDH in relation to the corresponding non-ischemic retinae analyzed by RT-PCR (n = 8; data are mean ± SD; IRI vs. IRI + ODQ + ALF-186 * = p < 0.05). c Representative Western Blot image (n = 8) showing the suppression of phosphorylated NF-κB compared to total NF-κB after immediate ALF-186 treatment. Enucleation was performed 24 h post IRI. d Densitometric analysis of n = 8 Western Blots for phosphorylated NF-κB after ALF-186 and ODQ inhibition (data are mean ± SD; IRI vs. IRI + ALF-186, * = p < 0.05, IRI + ALF-186 vs. IRI + ODQ + ALF-186, * = p < 0.05)Back to article page