Inhibition of Hydrogen Peroxide-Induced Human Umbilical Vein Endothelial Cells Aging by Allicin Depends on Sirtuin1 Activation

BACKGROUND: The abnormal activity of Sirtuin 1 (Sirt1) is closely related to the aging of vascular endothelial cells. As a bioactive molecule, allicin has antioxidant, anti-inflammatory, and lipid-regulating mechanisms. However, few reports about the relationship of allicin and Sirt1 have been published. In this study, we aimed to elucidate the effect of allicin on Human Umbilical Vein Endothelial Cells (HUVECs) aging induced by hydrogen peroxide (H(2)O(2)) and the role of Sirt1 in this phenomenon. MATERIAL/METHODS: HUVEC were exposed to H(2)O(2) to establish the aging model. The expression of protein and RNA were detected by Western blot and Reverse transcription-quantitative polymerase chain reaction. The 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to assess cell viability. Sirt1 enzyme activity assay was used to analyze enzymatic activity. Reactive oxygen species was detected by dichlorofluorescein diacetate (DCFH-DA). Cell aging was detected by Senescence β-Galactosidase (SA-β-gal) staining. RESULTS: Results of this study revealed that pretreating HUVECs with 5 ng/mL allicin before exposure to H(2)O(2) resulted in increased cell viability and reduced reactive oxygen species generation. Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) analysis showed that H(2)O(2) attenuated the phosphorylation and activation of Sirt1 and increased the expression of plasminogen activator inhibitor-1(PAI-1) protein. Moreover, H(2)O(2) also promoted HUVEC aging. These effects were significantly alleviated by 5 ng/mL allicin co-treatment. Furthermore, the anti-aging effects of allicin were abolished by the Sirt1 inhibitor nicotinamide (NAM). CONCLUSIONS: Overall, the results demonstrated that allicin protects HUVECs from H(2)O(2)-induced oxidative stress and aging via the activation of Sirt1.