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. Author manuscript; available in PMC: 2007 Sep 19.
Published in final edited form as: Curr Neurovasc Res. 2005 Dec;2(5):387–399. doi: 10.2174/156720205774962683

Fig. (6). Prevention of apoptotic genomic DNA fragmentation and cellular membrane PS exposure by EPO during β-amyloid (Aβ) toxicity is mediated by NF-κB p65.

Fig. (6)

(A) Neurons were transfected with NF-κB p65 siRNA for 72 hours prior to EPO and Aβ application. DNA fragmentation was assessed 24 hours after Aβ administration using TUNEL and PS exposure was determined by annexin V phycoerythrin labeling 24 hours following Aβ administration. Representative images illustrate DNA fragmentation and membrane PS externalization in neurons using transmitted (T) light and fluorescence (F) light of the same microscopy field with 490 nm excitation and 585 nm emission wavelengths. EPO (10 ng/ml) applied 1 hour prior to Aβ administration significantly prevented DNA fragmentation and membrane PS exposure following Aβ. In contrast, gene silencing of NF-κB p65 with siRNA abrogates protection of EPO in neurons and yields a significant increase in positive TUNEL and cellular membrane PS externalization. (B) NF-κB p65 gene silencing with targeted siRNA eliminates protection conferred by EPO against Aβ, resulting in an increase in percent DNA fragmentation and cellular membrane PS exposure (*P<0.01 vs. Aβ treated alone; †P<0.01 vs. EPO/Aβ). Each data point represents the mean and SEM. Control = untreated cultures.