"Gypenosides isolated from Gynostemma pentaphyllum are widely used in traditional Chinese medicine, with beneficial effects reported in numerous diseases, including inflammation and atherosclerosis, although the mechanism underlying these therapeutic effects is unknown. Because increased nitric oxide (NO) plays a role in these pathological conditions, we investigated whether the pharmacological activity of gypenosides is due to suppression of NO synthesis. The markedly increased production of nitrite by stimulation of RAW 264.7 murine macrophages with 1 microg/mL lipopolysaccharide (LPS) for 20 h (unstimulated: 0.3+/-0.3 microM vs. LPS: 32.5+/-1.2 microM) was dose-dependently inhibited by gypenosides (0.1-100 microg/mL). When cells were pretreated with gypenosides (for 1h) prior to LPS stimulation, subsequent NO production was significantly attenuated (IC(50) of 3.1+/-0.4 microg/mL) (P<0.05). Gypenosides (25 microg/mL) produced the same maximum inhibition of LPS-induced NO production as aminoguanidine, a standard inhibitor of NOS enzymes. Suppression of NO production occurred both by direct inhibition of the activity and expression of iNOS. Inhibition of iNOS protein expression appears to be at the transcriptional level, since gypenosides decreased LPS-induced NF-kappaB activity in a dose-dependent manner (P<0.05), with significant inhibition achieved following pretreatment with 10 microg/mL gypenoside. Taken together, these results suggest that gypenosides derived from G. pentaphyllum suppress NO synthesis in murine macrophages by inhibiting iNOS enzymatic activity and attenuating NF-kappaB-mediated iNOS protein expression, thereby implicating a mechanism by which gypenosides may exert their therapeutic effects." Read more

 

 

 

"The action of gypenosides (GP, saponins of Gynostemma pentaphyllum, a Chinese medicinal herb) as an antioxidant was studied using various models of oxidant stress in phagocytes, liver microsomes and vascular endothelial cells. The results show that GP decreased superoxide anion and hydrogen peroxide content in human neutrophils and diminished chemiluminescent oxidative burst triggered by zymosan in human monocytes and murine macrophages. An increase of lipid peroxidation induced by Fe2+/cysteine, ascorbate/NADPH or hydrogen peroxide in liver microsomes and vascular endothelial cells was inhibited by GP. It was also found that GP protected biomembranes from oxidative injury by reversing the decreased membrane fluidity of liver microsomes and mitochondria, increasing mitochondrial enzyme activity in vascular endothelial cells and decreasing intracellular lactate dehydrogenase leakage from these cells. The extensive antioxidant effect of GP may be valuable to the prevention and treatment of various diseases such as atherosclerosis, liver disease and inflammation." Read more

 

 

 

 

"Lipid peroxidation and toxicity associated with oxygen radicals have been suggested as major causes of cancer, atherosclerosis and the aging process. Damage of endothelial cells may lead to cardiovascular and cerebrovascular diseases. Endothelial cells are susceptible to oxidant insult. In the present study, the antioxidant effect of a Chinese medicinal herb, Gynostemma pentaphyllum Makino (Chinese name, Jiaogulan), was investigated in vitro using vascular endothelial cells. Confluent monolayers of bovine pulmonary artery endothelial cells (PAEC) were preincubated with different concentrations of gypenosides (GP, total saponins of Gynostemma pentaphyllum) for 16 h, then washed and incubated with hydrogen peroxide (H2O2) for 4 h. Cell injury was assessed by measuring the release of intracellular lactate dehydrogenase (LDH), and cell viability with tetrazolium (MTT) assay. Lipid peroxidation products of PAEC were monitored as thiobarbituric acid-reactive substances (TBARS) with a fluorometric assay. The results showed that 62.5 M H2O2 incubated with PAEC for 4 h increased the percentage of LDH release, decreased cell viability manifested by MTT absorbance at 620 nm, and elevated TBARS. Preincubation of GP (25-150 g/mL) with PAEC for 16 h before H2O2 exposure significantly declined LDH release, increased cell viability, and reduced TBARS. These results demonstrate that gypenosides can protect vascular endothelial cells from oxidant injury. The data thus suggest that gypenosides may be beneficial for the prevention and treatment of atherosclerosis and for retardation of the aging process." Read more