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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: 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 injury

Fig. 3

ALF-186 treatment increases sGC expression in retinal ganglion cells due to IRI a sGC and Brn3a/DAPI co-expression in the retina after unilateral IRI in the presence and abscence of ALF-186/iALF-186 or PBS. Cross-sections of the retinae 24 h after unilateral IRI. In controls with and without IRI sGC was only positive as a baseline expression. ALF-186 vehicle group and IRI + ALF-186 treatment resulted in an increased expression of sGC, mostly in the inner nuclear layer and the retinal ganglion cells as co-staining with Brn3a demonstrates (right column, forth image, arrows). Inactivated ALF-186 did not show any significant effects concerning sGC expression compared to control groups. (Scale bar, 50 μm; Abbreviations: NFL = nerve fiber layer, GCL = ganglion cell layer, INL = inner nuclear layer and ONL = outer nuclear layer). b Frequency density of sGC protein expression in the groups as quantified by histogram analysis (*** = p < 0.001 PBS vs. ALF-186 amd IRI + ALF-186 and IRI + ALF-186 vs. IRI + iALF-186)

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