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. Author manuscript; available in PMC: 2011 Aug 4.
Published in final edited form as: Curr Neurovasc Res. 2011 Aug 1;8(3):220–235. doi: 10.2174/156720211796558069

Fig. (4). EPO protects against EC injury through blocking apoptotic early phosphatidylserine (PS) exposure and nuclear DNA degradation in ECs during OGD.

Fig. (4)

(A and C) Representative images demonstrate that OGD led to a significant increase in percent trypan blue staining, DNA fragmentation, and membrane PS exposure in ECs at 24 hours after OGD compared to untreated control cultures, which was prevented by EPO (10 ng/ml), resveratrol (RES 15 μM) or EPO/RES combined application. Yet, inhibition of SIRT1 activity with EX527 (2 μM) or gene silence of SIRT1 with siRNA significantly increased apoptotic injury to a greater level during OGD and attenuated the efficacy of EPO. (B and D) Quantification of these results illustrate that EPO (10 ng/ml) application significant decreased percent trypan blue uptake, DNA fragmentation, and membrane PS exposure 24 hours after OGD when compared to OGD treated alone (*P < 0.01 vs. untreated control; †P <0.05 vs. OGD). Inhibition of SIRT1 activity with EX527 (2 μM) or gene silence of SIRT1 with siRNA significantly increased apoptotic injury to a greater level beyond OGD alone and attenuated the efficacy of EPO. Each data point represents the mean and SEM from 6 experiments.