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. Author manuscript; available in PMC: 2013 Feb 1.
Published in final edited form as: Eur J Neurosci. 2012 Jan 25;35(3-4):562–571. doi: 10.1111/j.1460-9568.2011.07972.x

Figure 7. p66-KO neurons showed greater protection following treatment with oxidative insults implicated in EAE and MS neurodegenerative pathways.

Figure 7

p66-KO neurons had a significantly greater cell viability percentage compared to WT neurons when treated for 15 minutes with either A) 500μ-M of DETA-NO or B) 200 μ-M H2O2. Cell counts were obtained 24 hours post treatment. A) DETA-NO treated p66-KO neurons had a mean cell viability of 94.7±1.2% compared to 64.0±14.6% for the WT neurons (p=0.04). B) H2O2 treated p66-KO neurons had a mean cell viability of 81.7±2.2% compared to 45.7±0.7% for the WT neurons (p=0.02). (n per treatment/genotype = 3 cultures; 4 plates/culture)