Previously, it was found that total saponins from panax notoginseng inhibited Ca2+ influx coupling to activation of alpha1-adrenoceptor. This study was designed to investigate the effects of ginsenoside-Rd from total saponins of panax notoginseng on receptor-operated (ROCC) and store-operated (SOCC) Ca2+ channels in vascular smooth muscle cells using fura-2 fluorescence, whole cell patch clamp ion channel recording, radio-ligand-receptor binding, 45Ca2+ radio-trace and organ bath techniques. It was found that ginsenoside-Rd reduced phenylephrine-induced contractile responses and Ca2+ influx in normal media without significant effect on these responses in Ca2+ -free media. Ginsenoside-Rd also decreased phenylephrine- and thapsigargin-induced inward Ca2+ currents, and attenuated thapsigargin- and 1-oleoy-2-acetyl-sn-glycerol (OAG)-induced cation entries that are coupled to ROCC and SOCC respectively. Ginsenoside-Rd failed to inhibit KCl-induced contraction of rat aortal rings and Ca2+ influx, and did not alter voltage-dependent inward Ca2+ current (VDCC) which was blocked by nifedipine. Also, ginsenoside-Rd did not change binding site and affinity of [3H]-prazosin for alpha1-adrenoceptor in the vascular plasma membrane. These results suggest that ginsenoside-Rd, as an inhibitor, remarkably inhibits Ca2+ entry through ROCC and SOCC without effects on VDCC and Ca2+ release in vascular smooth muscle cells.
"One research  suggested that PNS could increase Ca2+ level in endothelial cells via the receptor-operated Ca2+ channels in the presence of acetylcholine (ACh) or the nonselective cation channels opened by cyclopiazonic acid (CPA). Another research  indicated that ginsenoside-Rd could remarkably inhibit Ca2+ entry through receptor-operated calcium channel (ROCC) and store-operated calcium channel (SOCC) without effects on voltage-dependent inward Ca2+ current (VDCC) and Ca2+ release in vascular smooth muscle cells. Ginsenoside-Rd inhibited cell proliferation and reversed basilar artery remodeling , while Rb1 and Rg1 increased endothelial-dependent vessel dilatation through the activation of NO by modulating the PI3K/Akt/eNOS pathway and l-arginine transport in endothelial cell . "
[Show abstract][Hide abstract] ABSTRACT: Panax notoginseng saponins (PNS) are one of the most important compounds derived from roots of the herb Panax notoginseng which are traditionally used as a hemostatic medicine to control internal and external bleeding in China for thousands of years. To date, at least twenty saponins were identified and some of them including notoginsenoside R1, ginsenoside Rb1, and ginsenoside Rg1 were researched frequently in the area of cardiovascular protection. However, the protective effects of PNS on cardiovascular diseases based on experimental studies and its underlying mechanisms have not been reviewed systematically. This paper reviewed the pharmacology of PNS and its monomers Rb1, Rg1, and R1 in the treatment for cardiovascular diseases.
Evidence-based Complementary and Alternative Medicine 07/2014; 2014:204840. DOI:10.1155/2014/204840 · 1.88 Impact Factor
"Although the mechanisms responsible for ginseng's various effects remain largely unknown, several active ingredients termed ginsenosides have been isolated from the plant –. Ginsenoside Rd, Dammer-24(25)-ene-3β, 12β, 20(S)- triol-(20-O-β-D-glucopyranosyl)-3-O-β-D-glucopyranosyl-(1→2)-β-D-gluco-pyranoside (GSRd, C48H82O18·3H2O, molecular weight 1001, Figure 1), one of the major P. ginseng isolates, scavenges free radicals , , inhibits Ca2+-influx via receptor and store-operated Ca2+ channels , and protects against neuronal apoptosis , . Therefore, in addition to being highly lipophilic and capable of easily diffusing across biological membranes, GSRd may have significant advantageous cardiac effects. "
[Show abstract][Hide abstract] ABSTRACT: Evidence suggests Ginsenoside Rd (GSRd), a biologically active extract from the medical plant Panax Ginseng, exerts antioxidant effect, decreasing reactive oxygen species (ROS) formation. Current study determined the effect of GSRd on myocardial ischemia/reperfusion (MI/R) injury (a pathological condition where ROS production is significantly increased) and investigated the underlying mechanisms. The current study utilized an in vivo rat model of MI/R injury and an in vitro neonatal rat cardiomyocyte (NRC) model of simulated ischemia/reperfusion (SI/R) injury. Infarct size was measured by Evans blue/TTC double staining. NRC injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. ROS accumulation and apoptosis were assessed by flow cytometry. Mitochondrial membrane potential (MMP) was determined by 5, 5', 6, 6'-tetrachloro-1, 1', 3, 3'-tetrathylbenzimidazol carbocyanine iodide (JC-1). Cytosolic translocation of mitochondrial cytochrome c and expression of caspase-9, caspase-3, Bcl-2 family proteins, and phosphorylated Akt and GSK-3β were determined by western blot. Pretreatment with GSRd (50 mg/kg) significantly augmented rat cardiac function, as evidenced by increased left ventricular ejection fraction (LVEF) and ±dP/dt. GSRd reduced myocardial infarct size, apoptotic cell death, and blood creatine kinase/lactate dehydrogenase levels after MI/R. In NRCs, GSRd (10 µM) inhibited SI/R-induced ROS generation (P<0.01), decreased cellular apoptosis, stabilized the mitochondrial membrane potential (MMP), and attenuated cytosolic translocation of mitochondrial cytochrome c. GSRd inhibited activation of caspase-9 and caspase-3, increased the phosphorylated Akt and GSK-3β, and increased the Bcl-2/Bax ratio. Together, these data demonstrate GSRd mediated cardioprotective effect against MI/R-induced apoptosis via a mitochondrial-dependent apoptotic pathway.
PLoS ONE 08/2013; 8(8):e70956. DOI:10.1371/journal.pone.0070956 · 3.23 Impact Factor
"Previous studies have shown that Panax notoginseng mainly contained dammarane-type saponins (ginsenosides) including sanchinoside or notoginsenoside which is unique to Panax notoginseng [3–6]. Recent researches have revealed various pharmacological effects of notoginsenosides such as blocking Ca2+ influx through the receptor, enhancing astrocyte differentiation, and inhibiting vessel restenosis and antifibrotic effects [7–10]. "
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study is to investigate the effects of Borneol on the pharmacokinetics of notoginsenoside R1 (NGR1) and the ginsenosides Rg1 (GRg1) and Re (GRe) in Panax notoginseng. Reversed phase high-performance liquid chromatography coupled with electrospray ion trap mass spectrometry was employed to determine the concentrations of the three compounds in rabbit plasma. In comparison with rabbits administrated Panax notoginseng extract alone, animals simultaneously taking Panax notoginseng extract and Borneol exhibited significant differences in pharmacokinetic parameters of NGR1, GRg1, and GRe, such as increasing their bioavailability. Quantities of NGR1, GRg1, and GRe in rabbit tissues were also increased after combining administration of Borneol. In addition, the apparent permeability coefficients (P app) of NGR1, GRg1, and GRe were raised by Borneol significantly in Caco-2 cells. However, no significant changes were observed in the efflux ratio (Er) of NGR1, GRg1 and GRe. These data indicate that Borneol has the properties of enhancing the intestinal absorption, increasing the distribution, and inhibiting the metabolism of NGR1, GRg1, and GRe. The underlying mechanism might be attributed to the loosening of the intercellular tight junction.
Journal of Analytical Methods in Chemistry 03/2013; 2013(5):706723. DOI:10.1155/2013/706723 · 0.79 Impact Factor
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