Table 1: Cardiovascular effects of PNS (Rb1, Rg1, and R1) in vitro research.


NGPRP and rat washed platelets Antiplatelet, anticoagulant, and antithrombotic effect(i) Inhibit ADP-induced platelet aggregationYao et al., 2008 [3]
NGRat washed platelets(ii) Increase the levels of Grb2, thrombospondin 1, and tubulin alpha 6 and decrease the levels of thioredoxin, Cu-Zn superoxide dismutase, DJ-1 protein, peroxiredoxin 3, thioredoxin-like protein 2, ribonuclease inhibitor, potassium channel subfamily V member 2, myosin regulatory light chain 9, and laminin receptor 1Yao et al., 2008 [3]
         (iii) Decrease the ROS level    
NG-R1Cultured human endothelial cells from different vascular sources(iv) Increase the synthesis of t-PA and decrease PAI-1 activity Zhang et al., 1997 [12]

PNSH9c2 cells Protecting myocardium cells from apoptosis(i) Activate PI3K/Akt signaling pathwayChen et al., 2011 [13]
PNSH9c2 cells(ii) Lower the levels of serum LDH, CK, and CK-MB and normalize myocardial superoxide dismutase, glutathione peroxidase, and catalase activitiesShi et al., 2007 [24]
PNSCultured cardiomyocytes(iii) Alleviate intracellular calcium overloadChen et al., 2005 [23]

Radix notoginseng formulaHUVEsPromoting cardiac angiogenesisPromote HUVEC proliferation and secretion of VEGF, expression of VEGFR-2 proteinLei et al., 2010 [34]

Ginsenoside Rg1Rat cardiomyocyte H/R modelAntimyocardial ischemia and hypoxia effectReduce lactate dehydrogenase release and increased cell viability and reduce intracellular ROS and suppressed the intracellular Ca( +) levelZhu et al., 2009 [38]

Notoginseng extracts (ginsenoside Rg1 and ginsenoside Rb1)DCs 2.4 cellsInhibitory effect on the inflammatory responsesInhibition of TNF-alpha production and inhibit LPS-stimulated cytokine productionRhule et al., 2008 [46]

PNSVSMCs Inhibition of intimal hyperplasia and smooth muscle cell proliferation(i) Inhibit the activation of PDGF-induced P-ERK1/2 and increase the content of MKP-1Zhang et al., 2012 [49]
PNSVSMCs(ii) Upregulate p53, Bax, and caspase-3 expressions and downregulate Bcl-2 expressionXu et al., 2011 [50]
PNSVSMCs(iii) Inhibit the VSMC proliferation induced by hyperlipidemia serumLin et al., 1993 [51]
PNSVSMCs(iv) Inhibit the VSMC proliferation induced by hyperlipidemia serumWang et al., 2006 [8]

PNSApoE-KO mice Antiatherosclerosis effect(i) Lower the serum levels of lipid and oxLDL, ratio of plaque area to vessel area, and expression of CD40 and MMP-9Liu et al., 2009 [53]
PNSHUVEC(ii) Improve its activity, elevate the adhesion rate with monocytes, and increase the protein expression of ICAM-1Qin et al., 2008 [54]
       (iii) Decrease the mRNA expression levels of monocyte chemoattractant protein-1 and nuclear factor-kappaB/p65 Liu et al., 2010 [55]
PNS, ginsenoside Rg1, and ginsenoside Rb1HCAECs(iv) Inhibit TNF-alpha-induced NF-kappaB activationWang et al., 2011 [59]
PNSHUVECs (v) Regulate the VEGF-KDR/Flk-1 and PI3K-Akt-eNOS signaling pathwaysHong et al., 2009 [60]

PNSEndothelial cells Vasodilative effect(i) Increase of Ca2+ level via the receptor-operated Ca2+ channels in the presence of ACh or the nonselective cation channels opened by CPA C. Y. Kwan, and T. K. Kwan, 2000 [65]
Ginsenoside-RdVSMCs(ii) Inhibit Ca2+ entry through ROCC and SOCC without effects on VDCC and Ca2+ release Guan et al., 2006 [66]
Ginsenoside-RdBASMCs(iii) Inhibit cell proliferation and reverse basilar artery remodelingLi et al., 2012 [67]
Rb1 and Rg1Endothelial cell(iv) Increase endothelial-dependent vessel dilatation through the activation of NO by modulating the PI3K/Akt/eNOS pathway and l-arginine transport Pan et al., 2012 [68]

PNSCultured myocardial cellsInhibition of left ventricular remodelingInhibitory action on neurohormonal factor NEZhou et al., 2005 [71]

NG: notoginsengnosides; NG-R1: notoginsenoside R1; H/R: hypoxia/reoxygenation; DCs: dendritic cells; VSMCs: vascular smooth muscle cells; apoE-KO: apolipoprotein E-knockout; HUVEC: human umbilical vascular endothelial cells; HCAECs: human coronary artery endothelial cells; BASMCs: basilar artery smooth muscle cells; PRP: platelet rich plasma; Grb2: growth factor receptor-bound protein 2; ROS: reactive oxygen species; t-PA: plasminogen activator; PAI-1: plasminogen activator inhibitor-1; oxLDL: oxidized low density lipoprotein; ICAM-1: intercellular adhesion molecule-1; Ach: acetylcholine; CPA: cyclopiazonic acid; ROCC: receptor-operated; SOCC: store-operated; VDCC: voltage-dependent inward Ca2+ current.