Kim H, Chen X, Gillis C N
Department of Anesthesiology, Yale University School of Medicine, New Haven, CT 06510.
Biochem Biophys Res Commun. 1992 Dec 15;189(2):670-6. doi: 10.1016/0006-291x(92)92253-t.
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.
我们研究了人参皂甙对自由基诱导的肺内皮损伤的作用，这种损伤表现为在灌注的、血管收缩的肺中，对乙酰胆碱的正常血管舒张反应发生逆转。50或200微克/毫升的人参皂甙可预防这种损伤反应，并减轻自由基损伤后的肺水肿，但不改变完整肺中正常的乙酰胆碱诱导的血管舒张。在用U46619预收缩的对照灌注肺中，人参皂甙混合物或纯化的人参皂甙Rb1和Rg1引起血管舒张。一氧化氮合酶抑制剂100微摩尔硝基-L-精氨酸消除了这种作用。在培养的牛主动脉内皮细胞中，人参皂甙（10微克/毫升）刺激[14C]-L-精氨酸转化为[14C]-L-瓜氨酸。这些数据表明，人参皂甙可能通过促进一氧化氮的释放而引起血管舒张，并预防氧自由基损伤的表现。
