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Fig. 5 | Journal of Neuroinflammation

Fig. 5

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. 5

Effect of ALF-186 treatment on retinal protein and mRNA expression of TNF-α in tissue and TNF-α serum levels. a Fold induction of TNF-α mRNA expression after ALF-186 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 + ALF-186 + ODQ, * = p < 0.05). b + c Representative Western Blot image and densitometric analysis of n = 8 Western Blots showing the suppression of retinal cleavage of TNF-α compared to β-Actin after ALF-186 (data are mean ± SD; IRI vs. IRI + ALF-186, *** = p < 0.001) and it’s clearing after ODQ treatment (IRI + ALF-186 vs. IRI + ALF-186 + ODQ, * = p < 0.05). d Histological images, showing that TNF-α protein expression is increased due to IRI + PBS, while ALF-186 treatment attenuates this effect. Quantification via frequency density of TNF-α protein expression in both groups by histogram analysis revealed a significant downregulation of TNF-α due to ALF-186 treatment (p < 0.001). e TNF-α serum levels in peripheral blood serum after ALF-186 treatment (data are mean ± SD; n = 8; Sham vs. IRI, *** = p < 0.001; IRI vs. IRI + ALF-186, ** = p < 0.01 and IRI + ALF-186 vs. ODQ + IRI + ALF186, * = p < 0.05)

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Journal of Neuroinflammation

ISSN: 1742-2094