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Ad-SIRT1 induced NO production via the PI3K/Akt/eNOS signaling pathway. The intracellular NO level was elevated after treatment with Ad-SIRT1. Pretreatment of EPCs with LY294002 (30 μM), sc-221226 (30 μM), or L-NAM (200 μM) downregulated Ad-SIRT1-induced NO production in EPCs, in comparison with the controls (*P < 0.05 vs. control, #P < 0.05 vs. Ad-SIRT1).
