Table 1.
Cardiovascular effects of PNS (Rb1, Rg1, and R1) in vitro research.
| Compounds | Cells/tissues | Effects | Study | |
|---|---|---|---|---|
| NG | PRP and rat washed platelets | Antiplatelet, anticoagulant, and antithrombotic effect | (i) Inhibit ADP-induced platelet aggregation | Yao et al., 2008 [3] |
| NG | Rat 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 1 | Yao et al., 2008 [3] | |
| (iii) Decrease the ROS level | ||||
| NG-R1 | Cultured human endothelial cells from different vascular sources | (iv) Increase the synthesis of t-PA and decrease PAI-1 activity | Zhang et al., 1997 [12] | |
|
| ||||
| PNS | H9c2 cells | Protecting myocardium cells from apoptosis | (i) Activate PI3K/Akt signaling pathway | Chen et al., 2011 [13] |
| PNS | H9c2 cells | (ii) Lower the levels of serum LDH, CK, and CK-MB and normalize myocardial superoxide dismutase, glutathione peroxidase, and catalase activities | Shi et al., 2007 [24] | |
| PNS | Cultured cardiomyocytes | (iii) Alleviate intracellular calcium overload | Chen et al., 2005 [23] | |
|
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| Radix notoginseng formula | HUVEs | Promoting cardiac angiogenesis | Promote HUVEC proliferation and secretion of VEGF, expression of VEGFR-2 protein | Lei et al., 2010 [34] |
|
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| Ginsenoside Rg1 | Rat cardiomyocyte H/R model | Antimyocardial ischemia and hypoxia effect | Reduce lactate dehydrogenase release and increased cell viability and reduce intracellular ROS and suppressed the intracellular [Ca(2+)] level | Zhu et al., 2009 [38] |
|
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| Notoginseng extracts (ginsenoside Rg1 and ginsenoside Rb1) | DCs 2.4 cells | Inhibitory effect on the inflammatory responses | Inhibition of TNF-alpha production and inhibit LPS-stimulated cytokine production | Rhule et al., 2008 [46] |
|
| ||||
| PNS | VSMCs | 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-1 | Zhang et al., 2012 [49] |
| PNS | VSMCs | (ii) Upregulate p53, Bax, and caspase-3 expressions and downregulate Bcl-2 expression | Xu et al., 2011 [50] | |
| PNS | VSMCs | (iii) Inhibit the VSMC proliferation induced by hyperlipidemia serum | Lin et al., 1993 [51] | |
| PNS | VSMCs | (iv) Inhibit the VSMC proliferation induced by hyperlipidemia serum | Wang et al., 2006 [8] | |
|
| ||||
| PNS | ApoE-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-9 | Liu et al., 2009 [53] |
| PNS | HUVEC | (ii) Improve its activity, elevate the adhesion rate with monocytes, and increase the protein expression of ICAM-1 | Qin 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 Rb1 | HCAECs | (iv) Inhibit TNF-alpha-induced NF-kappaB activation | Wang et al., 2011 [59] | |
| PNS | HUVECs | (v) Regulate the VEGF-KDR/Flk-1 and PI3K-Akt-eNOS signaling pathways | Hong et al., 2009 [60] | |
|
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| PNS | Endothelial 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-Rd | VSMCs | (ii) Inhibit Ca2+ entry through ROCC and SOCC without effects on VDCC and Ca2+ release | Guan et al., 2006 [66] | |
| Ginsenoside-Rd | BASMCs | (iii) Inhibit cell proliferation and reverse basilar artery remodeling | Li et al., 2012 [67] | |
| Rb1 and Rg1 | Endothelial 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] | |
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| PNS | Cultured myocardial cells | Inhibition of left ventricular remodeling | Inhibitory action on neurohormonal factor NE | Zhou 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.