Protective Effects of Ginsenoside Rb1 on Human Umbilical Vein Endothelial Cells In Vitro

Abstract

Ginseng has beneficial effects on the cardiovascular system, but its underlying mechanism is unclear. This study investigated the effects of ginsenoside Rb1, a major constituent of ginseng, on the changes of lactate dehydrogenase (LDH) activity, nitric oxide (NO), tissue-type plasminogen activator (t-PA), and plasminogen activator inhibitor-1 (PAI-1) in oxidized low-density lipoprotein (oxLDL)-injuring endothelial cells. Human umbilical vein endothelial cells were cultured and divided into 6 groups (n = 6): control group, oxLDL alone group (100 mg/L), ginsenoside Rb1 alone group (10 microg/mL), oxLDL plus ginsenoside Rb1 groups (0.1, 1.0, and 10 microg/mL, respectively.). Twenty-four hours after treatment, LDH activity and concentrations of NO, t-PA, and PAI-1 in culture medium were measured while the expressions of endothelial nitric oxide synthase (eNOS), t-PA, and PAI-1 mRNA in endothelial cells were detected by reverse-transcriptase polymerase chain reaction. Compared with control group, oxLDL (100 mg/L) caused LDH activity, the expressions of eNOS and t-PA mRNA, and concentrations of NO and t-PA to significantly decrease (P < 0.05, respectively), and it also led to dramatic increase of PAI-1 mRNA and concentration (P < 0.05, respectively). Ginsenoside Rb1 alone did not demonstrate this ability. High-dose Rb1 (10 microg/mL) could block the effects of oxLDL on LDH activity, mRNA of eNOS, t-PA, and PAI-1, and concentrations of NO, t-PA, and PAI-1 (P < 0.05, respectively), and neither low-dose Rb1 (0.1 microg/mL) nor medium-dose Rb1 (1.0 microg/mL) demonstrated this ability. We conclude that ginsenoside Rb1 has protective effects on oxLDL-injuring human vascular endothelial cells and can reverse the effects of oxLDL on NO, t-PA, and PAI-1.

Ginsenoside Rb1 Reduces Nitric Oxide Production via Inhibition of Nuclear Factor-κB Activation in Interleukin-1β- Stimulated SW1353 Chondrosarcoma Cells

“…It was also shown to abate homocysteine-induced endothelial dysfunction by increasing NO production and eNOS phosphorylation via PI3K/Akt activation and PKC inhibition [16]. Ginsenoside Rb1 had protective effects on oxLDL-injuring human vascular endothelial cells by increasing NO production and eNOS mRNA expressions [14]. Although these results appear to contradict our results, it is possible that regulation of NOS/NO signal by ginsenoside Rb1 varies in different pathological conditions.…”

“…Ginsenoside Rb1 inhibited the expression of TNF-α, IL-1β and IL-6 in lipopolysaccharide (LPS) -stimulated murine peritoneal macrophages [13]. Although release of NO by ginsenoside Rb1 may underlie the cardiovascular protection [14], the effects and mechanisms of ginsenoside Rb1 on NO production by chondrocytes during inflammatory conditions are not clear. Thus, the purpose of this study was to investigate the effect of ginsenoside Rb1 on NO production, iNOS expression and NF-κB activation in IL-1β-stimulated SW1353 chondrosarcoma cells.…”

The Human Paraoxonase Gene Cluster As a Target in the Treatment of Atherosclerosis

“…OxLDL can also induce increased production of intracellular ROS and apoptosis by binding to lectin-like oxLDL receptor-1 (65, 72). OxLDL also affects the expression of various key genes in endothelial cells, thus altering endothelial function (126). In addition, oxLDL can also induce cytoskeletal rearrangements such as F-actin distribution, cell contraction, and the formation of intercellular gaps (92,364).…”

Protective Effects and Active Ingredients of Yi-Qi-Fu-Mai Sterile Powder Against Myocardial Oxidative Damage in Mice

“…Some papers had reported that ginsenoside Re can protect cardiomyocytes from oxidant injury induced by both exogenous and endogenous oxidants through scavenging H 2 O 2 and hydroxyl radicals (35). Ginsenoside Rb1 has been shown to protect against myocardial-reperfusion injury by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress and protecting the endothelial cells (36,37). Ginsenoside Rg1 has been reported to promote endogenous NO production, prolong ventricular refractoriness and repolarization, and inhibit left ventricular (LV) hypertrophy in rats (38).…”