Ginsenosides protect pulmonary vascular endothelium against free radical-induced injury.

We studied the actions of saponin (ginsenosides) from Panax ginseng on free radical-induced pulmonary endothelial injury which is manifest as reversal of the normal vasodilator response to acetylcholine in perfused, vasoconstricted lungs. 50 or 200 micrograms/ml ginsenosides prevented this injury response and also reduced the pulmonary edema which follows free radical injury but did not alter the normal ACh-induced vasodilation in intact lungs. In control perfused lungs preconstricted with U46619, the ginsenoside mixture or purified ginsenosides Rb1 and Rg1 caused vasodilatation. This effect was eliminated by 100 microM nitro-L-arginine, an inhibitor of nitric oxide synthase. In cultured bovine aortic endothelial cells, ginsenosides (10 micrograms/ml) stimulated the conversion of [14C]-L-arginine to [14C]-L-citrulline. These data indicate that GS may cause vasorelaxation and prevent manifestations of oxygen free radical injury by promoting release of nitric oxide.