Administration of polysaccharide from Panax notoginseng prolonged the survival of H22 tumor-bearing mice.

PMID: 
Onco Targets Ther. 2016 ;9:3433-41. Epub 2016 Jun 8. PMID: 27354815 Abstract Title: 
Administration of polysaccharide from Panax notoginseng prolonged the survival of H22 tumor-bearing mice. Abstract: 
BACKGROUND: Polysaccharides from various sources are being considered potential sources for the treatment of liver cancer. The aim of this study was to investigate the impact of polysaccharide isolated from Panax notoginseng (PPN) on the proliferation of H22 liver cancer cells and the survival of the tumor-bearing mice transplanted with H22 cells.MATERIALS AND METHODS: Polysaccharide from PPN was added to the culture medium of mouse hepatoma H22 cells at different doses. Cell proliferation was assayed with a standard MTT assay. Survival rates of tumor-bearing mice were recorded. Peripheral blood lymphocytes were assayed by flow cytometry. Serum interleukin-2 levels in peripheral blood were measured by enzyme-linked immunosorbent assay.RESULTS: Polysaccharide from PPN inhibited the growth of H22 cells and significantly prolonged the survival of tumor-bearing mice. The increase in activated CD4(+) T-cells and the elevation of serum interleukin-2 may contribute to the antitumor activity of PPN.CONCLUSION: PPN has potential antitumor activity for the treatment of liver cancer. read more

Panax notoginseng saponins provided neuroprotective effects in a rat model of cerebral ischemia.

PMID: 
J Ethnopharmacol. 2016 Aug 22 ;190:301-12. Epub 2016 Jun 8. PMID: 27288754 Abstract Title: 
Panax notoginseng saponins provide neuroprotection by regulating NgR1/RhoA/ROCK2 pathway expression, in vitro and in vivo. Abstract: 
ETHNOPHARMACOLOGICAL RELEVANCE: Panax notoginseng saponins (PNS) extracted from a traditional Chinese herbal medicine, Panax notoginseng (Burkill) F.H. Chen (Araliaceae), which has been extensively used in treating coronary heart disease, ischemic cerebrovascular disease and hemorrhagic disorders in China over hundreds of years.AIMS OF THE STUDY: This study explored whether panax notoginseng saponins (PNS) provided neuroprotective effects by inhibiting the expressions of NgR1, RhoA, and ROCK2 following middle cerebral artery occlusion in rats and oxygen-glucose deprivation/reoxygenation (OGD/R) injury in SH-SY5Y cells.MATERIALS AND METHODS: 2,3,5-Triphenyltetrazolium chloride staining was used to determine successful middle cerebral artery occlusion establishment in sham-operated and operated Sprague-Dawley rats 1 day after injury. The rats were randomly separated into sham, model, NEP1-40, PNS, and NEP1-40 plus PNS (N+P) groups. After 7 days of treatment, body mass and neurological deficit scores were analyzed. Tissues were harvested and analyzed by hematoxylin-eosin staining and immunohistochemical analysis, western blotting, and quantitative real-time PCR (qRT-PCR). The optimal drug concentration of NEP1-40 and PNS on SH-SY5Y cells exposed to OGD/R injury was determined by CCK8 analysis. qRT-PCR was used to measure mRNA expression profiles of NgR1, RhoA, and ROCK2 in SH-SY5Y cells subjected to OGD/R.RESULTS: The results showed that MCAO surgery successfully produced an infarct, and the PNS, NEP1-40, and N+P groups exhibited increased body mass and ameliorated neurological deficits compared with the model group. NEP1-40 treatment markedly reduced NgR1 and RhoA overexpression when compared to the model group, although there was no significant difference in ROCK2 expression. PNS and N+P treatment significantly decreased NgR1, RhoA, and ROCK2 overexpression compared with the model group. However, N+P treatment did not result in a synergistic effect, as assessed by immunohistochemistry, western blotting, and qRT-PCR. Following optimal administration of PNS (160μg/ml) and NEP1-40 (10ng/ml) on SH-SY5Y cells exposed to OGD/R injury, cell viability in the NEP1-40, PNS, and N+P groups significantly increased compared with the model group, as assessed by CCK8 analysis. Additionally, NgR1, RhoA, and ROCK2 mRNA expression profiles were significantly less in theNEP1-40, PNS, and N+P groups compared with the model group.CONCLUSION: PNS provided neuroprotective effects in a rat model of cerebral ischemia and SH-SY5Y cells exposed to oxygen/glucose deprivation injury by inhibiting the overexpression of NgR1, RhoA, and ROCK2. read more

These results indicate that notoginsenoside R1 protects the heart against ischemia-reperfusion injury.

PMID: 
Exp Ther Med. 2016 Jun ;11(6):2341-2348. Epub 2016 Apr 4. PMID: 27284318 Abstract Title: 
Cardioprotective effect of notoginsenoside R1 in a rabbit lung remote ischemic postconditioning model via activation of the TGF-β1/TAK1 signaling pathway. Abstract: 
Pharmacological postconditioning using cardioprotective agents is able to reduce myocardial infarct size. Notoginsenoside R1 (NG-R1), a phytoestrogen isolated fromsaponins (PNS), is considered to have anti-oxidative and anti-apoptotic properties. However, its cardioprotective properties and underlying mechanisms remain largely unknown. The aim of the present study was to determine the cardioprotective and anti-apoptotic effects of NG-R1 in an ischemia-reperfusion (IR)-induced myocardial injury rabbit model. A total of 45 Japanese big-ear rabbits were equally randomized to three groups: Control group, remote ischemic postconditioning (RIP) group and NG-R1 intervention group. At the endpoint of the experiment, the animals were sacrificed to remove myocardial tissues for the detection of transforming growth factor (TGF)-β1-TGF-β activated kinase 1 (TAK1) pathway-related proteins by immunohistochemistry and western blot analysis, the activities of caspase-3, -8 and -9 in myocardial cells by fluorometric assay, and the apoptosis of myocardial cells by terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling. Right and left lung tissues were stained with hematoxylin and eosin (H&E) to observe the severity of injury. NG-R1 treatment reduced the activity of superoxide dismutase, increased the content of malondialdehyde, reduced the activities of caspase-3, -8 and -9, and inhibited the apoptosis of myocardial cells in rabbits undergoing RIP. In addition, the expression of TGF-β1-TAK1 signaling pathway-related proteins was downregulated following NG-R1 intervention. H&E staining of bilateral lung tissues showed that cell morphology was generally intact without significant alveolar congestion, and there was no significant difference among the three groups. These results indicate that NG-R1 protects the heart against IR injury, possibly by inhibiting the activation of the TGF-β1-TAK1 signaling pathway and attenuating apoptotic stress in the myocardium. read more

Panax notoginseng could inhibit the metastasis of human colorectal cancer cells.

PMID: 
Am J Chin Med. 2016 ;44(4):851-70. Epub 2016 May 24. PMID: 27222068 Abstract Title: 
Effects of Panax notoginseng on the Metastasis of Human Colorectal Cancer Cells. Abstract: 
The goal of this study was to investigate the effect of the Panax notoginseng ethanol extract (PNEE) on the regulation of human colorectal cancer (CRC) metastasis. The migratory, invasive, and adhesive abilities and the expression of metastasis-associated regulatory molecules in cultured human CRC cells (HCT-116) treated with the PNEE were analyzed in this study. The migratory and invasive abilities of HCT-116 cells were reduced after PNEE treatment. The incubation of HCT-116 cells with the PNEE for 24 h decreased MMP-9 expression and increased E-cadherin expression compared with the control group. The adhesion reaction assay indicated that treatment with the PNEE led to significantly decreased HCT-116 adhesion to endothelial cells (EA.hy926 cells). The integrin-1 protein levels in HCT-116 cells were significantly decreased following treatment with the PNEE. Similarly, the protein levels of E-selectin and intercellular adhesion molecule-1 (ICAM-1) were significantly decreased by treatment of the EA.hy926 endothelial cells with PNEE. A scanning electron microscope (SEM) examination indicated that HCT-116 cells treated with LPS combined with the PNEE had a less flattened and retracted shape compared with LPS-treated cells, and this change in shape was found to be a phenomenon of extravasation invasion. The transepithelial electrical resistance (TEER) of the EA.hy926 endothelial cell monolayer increased after incubation with the PNEE for 24 h. A cell-cell permeability assay indicated that HCT-116 cells treated with the PNEE displayed significantly reduced levels of phosphorylated VE-cadherin (p-VE-cadherin). These results demonstrate the antimetastatic properties of the PNEE and show that the PNEE affects cells by inhibiting cell migration, invasion, and adhesion and regulating the expression of metastasis-associated signaling molecules. read more