Shujie Yu

Ginsenoside Rb1 Prevents H2O2-Induced HUVEC Senescence by Stimulating Sirtuin-1 Pathway

Purposes We have previously reported that Ginsenoside Rb1 may effectively prevent HUVECs from senescence, however, the detailed mechanism has not demonstrated up to now. Recent studies have shown that sirtuin-1 (Sirt1) plays an important role in the development of endothelial senescence. The purpose of this study was to explore whether Sirt1 is involved in the action of Ginsenoside Rb1 regarding protection against H2O2-induced HUVEC Senescence. Methods and Results Senescence induced by hydrogen peroxide (H2O2) in human umbilical vein endothelial cells (HUVECs) was examined by analyzing plasminogen activator inhibitor-1 (PAI-1) expression, cell morphology, and senescence-associated beta-galactosidase (SA-β-gal) activity. The results revealed that 42% of control-treated HUVECs were SA-β-gal positive after treatment by 60 µmol/L H2O2, however, this particular effect of H2O2 was decreased more than 2-fold (19%) in the HUVECs when pretreated with Rb1 (20 µmol/L) for 30 min. Additionally, Rb1 decreased eNOS acetylation, as well as promoted more NO production that was accompanied by an increase in Sirt1 expression. Furthermore, upon knocking down Sirt1, the effect of Rb1 on HUVEC senescence was blunted. Conclusions The present study indicated that Ginsenoside Rb1 acts through stimulating Sirt1 in order to protect against endothelial senescence and dysfunction. As such, Sirt1 appears to be of particular importance in maintaining endothelial functions and delaying vascular aging.

ASSA14-11-01 Decreased the Expressions of Soluble VEGFR2 and SOD in Hypertensive Diabetic Patients

Objective To evaluate the expressions of soluble vascular endothelial growth factor receptor 2 (sVEGFR2) and superoxide dismutase (SOD) in plasma of hypertensive diabetic patients. Methods In this cross-sectional study, fifty-seven cases were enrolled, which were divided into hypertensive diabetic group (n = 31) and control group (n = 26). Blood pressure (BP) was obtained from each participant with mercury sphygmomanometer. The expressions of sVEGFR2 and SOD were measured by ELISA. Serum lipid profile, glucose and glycosylated haemoglobin A1C (GHbA1c) levels were detected. Results The levels of total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), body mass index (BMI), waist circumference were significantly higher in the hypertensive diabetic group than those in control group (p < 0.05). The mean plasma levels of sVEGFR2 and SOD in hypertensive diabetic group were significantly decreased compared to that in the normal group (p < 0.05). There was a significantly positive correlation between sVEGFR2 and SOD in the whole study population (r = 0.289, p < 0.05). Conclusions Soluble VEGFR2 and SOD expressions are decreased in hypertensive diabetic patients. This study indicates that decreased SOD expression may contribute to the reduction of sVEGFR2. Angiogenesis in these patients is impaired. So sVEGFR2 in plasma may be used as a biomarker to assess angiogenesis impairment in patients with hypertension and diabetes.