Administration of 4-(<i>α</i>-L-Rhamnosyloxy)-benzyl Isothiocyanate Delays Disease Phenotype in SOD1<sup>G93A</sup> Rats: A Transgenic Model of Amyotrophic Lateral Sclerosis

<div>GMG-ITC treatment promotes Nrf-2 activity and reduces PARP-1 activity. Nrf2 IHC localization shows a negative expression in brain sections sampled from untreated SOD1tg rats (a), while GMG-ITC administration stimulates Nrf2 nuclear activity (b) preserving tissue damage by prooxidative gene expression. PARP-1 immunodetection shows a positive staining in untreated SOD1tg rats (c) and an IHC negative localization in GMG-ITC treated SOD1tg rats (d).</div>

BioMed Research International

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Figure 9

Figure 9: Administration of 4-(<i>α</i>-L-Rhamnosyloxy)-benzyl Isothiocyanate Delays Disease Phenotype in SOD1<sup>G93A</sup> Rats: A Transgenic Model of Amyotrophic Lateral Sclerosis 

Figure 9 | Administration of 4-(α-L-Rhamnosyloxy)-benzyl Isothiocyanate Delays Disease Phenotype in SOD1G93A Rats: A Transgenic Model of Amyotrophic Lateral Sclerosis 