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OBJECTIVE@#To investigate whether ginsenoside Rb1 (Rb1) can protect human umbilical vein endothelial cells (HUVECs) against high glucose-induced apoptosis and examine the underlying mechanism.@*METHODS@#HUVECs were divided into 5 groups: control group (5.5 mmol/L glucose), high glucose (HG, 40 mmol/L) treatment group, Rb1 (50 µ mol/L) treatment group, Rb1 plus HG treatment group, and Rb1 and 3-(@*RESULTS@#Rb1 ameliorated survival in cells in which apoptosis was induced by high glucose (P<0.05 or P<0.01). Upon the addition of Rb1, mitochondrial and intracellular reactive oxygen species generation and malondialdehyde levels were decreased (P<0.01), while the activities of antioxidant enzymes were increased (P<0.05 or P<0.01). Rb1 preserved the mitochondrial membrane potential and reduced the release of Cyt-c from the mitochondria into the cytosol (P<0.01). In addition, Rb1 upregulated mitochondrial biogenesis-associated proteins (P<0.01). Notably, the cytoprotective effects of Rb1 were correlated with SIRT3 signalling pathway activation (P<0.01). The effect of Rb1 against high glucose-induced mitochondria-related apoptosis was restrained by 3-TYP (P<0.05 or P<0.01).@*CONCLUSION@#Rb1 could protect HUVECs from high glucose-induced apoptosis by promoting mitochondrial function and suppressing oxidative stress through the SIRT3 signalling pathway.
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AIM:To explore the role of Sirt1/eNOS signalling pathway in the protective effect of hydrogen sul-phide(H2S)against endothelial cell senescence induced by high glucose.METHODS:High glucose(33 mmol/L)was applied to induce senescence in primary human umbilical vein endothelial cells(HUVECs).The cell viability,the propor-tion of senescence-associated β-galactosidase(SA-β-Gal)positive cells and the plasminogen activator inhibitor 1(PAI-1) expression were detected to assess the senescence model.Mean while,Sirt1 siRNA was used to examine the effect of Sirt 1 on eNOS expression and the senescence-related parameters.RESULTS: Treatment of HUVECs with high glucose de-creased the cell viability slowly with a larger proportion of the cells stained with SA-β-Gal, and the protein expression of PAI-1 was dramatically increased.The increased cell viability,reduced SA-β-Gal positive cells and decreased protein ex-pression of PAI-1 were detected after sodium hydrosulfide(NaHS,100 μmol/L)treatment.Furthermore,NaHS treatment upregulated the protein expression of Sirt 1 and eNOS,and eventually increased the production of nitric oxide(NO).CON-CLUSION:Exogenous H2S modulates Sirt1/eNOS/NO pathway to prevent HUVECs against high glucose-induced senes-cence.