摘要：

n-3-Polyunsaturated fatty acids (PUFAs) protect against myocardial infarction, arteriosclerosis and high blood pressure by stimulating endothelial nitric oxide synthase (eNOS) to increase nitric oxide (NO) production. However, the mechanism remains to be elucidated. This study investigated the role of \\{SIRT1\\} in the protective effects of docosahexaenoic acid (DHA) in vascular endothelial cells. Exposure of human umbilical vein endothelial cells (HUVECs) to 0.3–30 μM \\{DHA\\} did not affect cell viability, and \\{DHA\\} treatment dose-dependently increased \\{SIRT1\\} expression. The DHA-mediated increase in \\{SIRT1\\} expression induced eNOS deacetylation, increasing endothelial NO. However, inhibition of \\{SIRT1\\} inhibited DHA-mediated increases in \\{NO\\} production. This effect was mediated via deacetylation of lysines 496 and 506 in the eNOS calmodulin-binding domain. The effects of \\{DHA\\} were also demonstrated in rat aortic rings, in which \\{DHA\\} treatment increased \\{SIRT1\\} expression and bioavailable NO. Our results demonstrate that \\{SIRT1\\} plays an important role in DHA-mediated increases in bioavailable \\{NO\\} via decreased eNOS acetylation.

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