Ginsenoside Ro

1 Panax sp.

Ginsenoside Ro exhibits a Ca2+-antagonistic antiplatelet effect with an IC50 of 155  μM. Ginsenoside Ro reduces the production of TXA2 more than it reduces the activities of COX-1 and TXAS.

In Vitro:Ginsenoside Ro in Panax ginseng is a beneficial novel Ca2+-antagonistic compound and may prevent platelet aggregation-mediated thrombotic disease. Ginsenoside Ro dose-dependently reduces thrombin-stimulated platelet aggregation, and IC50 is approximately 155 μM[1]. Ginsenoside Ro inhibits TXA2 production to abolish thrombin-induced platelet aggregation. Thromboxane A2 (TXA2) induces platelet aggregation and promotes thrombus formation. Ginsenoside Ro dose-dependently (50-300 μM) reduces the TXB2 level that is induced by thrombin; Ginsenoside Ro (300 μM) inhibits the thrombin-mediated elevation in TXB2 level by 94.9%. COX-1 activity in the absence of Ginsenoside Ro (negative control) is 2.3±0.1 nmol/mg protein. However, Ginsenoside Ro dose-dependently (50-300 μM) reduces its activity; at 300 μM, COX-1 activity is reduced by 26.4% of that of the negative control. TXA2 synthase (TXAS) activity in the absence of Ginsenoside Ro (negative control) is 220.8±1.8 ng/mg protein/min. However, Ginsenoside Ro dose-dependently (50-300 μM) reduces its activity; at 300 μM, TXAS activity is reduced by 22.9% of that of the negative control. The inhibitory effect of Ginsenoside Ro (300 μM) on TXB2 production (94.9%) is significantly higher than those on COX-1 (26.4%) and TXAS (22.9%) activities[2]. To assess the toxicity of Ginsenoside Ro in Raw 264.7 cells, they are first treated with various concentrations (10 μM, 50 μM, 100 μM, and 200 μM) of Ginsenoside Ro for 24 h. Ginsenoside Ro exhibits no significant dose dependent toxicity. The effect of Ginsenoside Ro is next determined on cell viability and ROS levels, a marker of oxidative stress, following treatment with 1 μg/mL LPS. LPS reduces cell viability by ∼70% compared with nontreated controls. Pretreatment with 100 μM and 200 μM Ginsenoside Ro for 1 h prior to 1 μg/mL LPS incubation for 24 h leads to a significant increase in cell viability. The changes in ROS levels and NO production are consistent with the effects of Ginsenoside Ro on viability[3].

In Vivo:Ginsenoside Ro dissolved in water is administrated by gavage to mice at doses of 25 and 250 mg/kg/day for 4 days before i.v. injection of HT29 in order to keep blood concentrations of Ginsenoside Ro above a certain level before HT29 i.v. injection followed by 40 days of oral administration of Ginsenoside Ro to the mice. After 38 days of treatment, the animals are euthanized, and the number of pulmonary metastatic nodules is counted in addition to evaluation of toxicity of Ginsenoside Ro and mouse pathology by HT29. Ginsenoside Ro (250 mg/kg/day) produces a significant decrease in the number of tumor nodules on the lung surface, yielding inhibition rates of 88% (P < 0.01)[4].

References:
[1]. Kwon HW, et al. Inhibitory Effects of Cytosolic Ca2+ Concentration by Ginsenoside Ro Are Dependent on Phosphorylation of IP3RI and Dephosphorylation of ERK in Human Platelets. Evid Based Complement Alternat Med. 2015;2015:764906. [2]. Jung-HaeShin, et al. Inhibitory effects of thromboxane A2 generation by ginsenoside Ro due to attenuation of cytosolic phospholipase A2 phosphorylation and arachidonic acid release. J Ginseng Res. 9 Jan 2018. [3]. Kim S, et al. Upregulation of heme oxygenase-1 by ginsenoside Ro attenuates lipopolysaccharide-induced inflammation in macrophage cells. J Ginseng Res. 2015 Oct;39(4):365-70. [4]. Jiang Z, et al. The traditional Chinese medicine Achyranthes bidentata and our de novo conception of its metastatic chemoprevention: from phytochemistry to pharmacology. Sci Rep. 2017 Jun 20;7(1):3888.

Anti-hepatitic activity of ginsenoside Ro.[Pubmed:1818342]

Planta Med. 1991 Dec;57(6):523-6.

Ginsenoside Ro, an oleanane-type saponin has been screened for activity in experimental models of acute and chronic hepatitis. Ginsenoside Ro (50 and 200 mg/kg, p.o.) inhibited the increase of serum glutamic oxaloacetic transaminase (s-GOT) and serum glutamic pyruvic transaminase (s-GPT) levels in D-galactosamine (GalN)- and carbon tetrachloride (CCl4)-induced acute hepatitic rats. Ginsenoside Ro inhibited the increase of connective tissue in the liver of CCl4-induced chronic hepatitic rats. Ginsenoside Ro showed a stronger inhibitory effect on the GalN-induced acute hepatitic model than those of the aglycone of Ginsenoside Ro, oleanolic acid, or glycyrrhizic acid and its aglycone, glycyrrhetinic acid.

Ginsenoside Ro suppresses interleukin-1beta-induced apoptosis and inflammation in rat chondrocytes by inhibiting NF-kappaB.[Pubmed:25908625]

Chin J Nat Med. 2015 Apr;13(4):283-9.

This study investigated effects of Ginsenoside Ro (Ro) on interleukin-1beta (IL-1beta)-induced apoptosis and inflammation in rat chondrocytes. The rat chondrocytes were co-treated with IL-1beta (10 ng.kg(-1)) and Ro (50, 100 and 200 mumol.L(-1)) for 48 h. Chondrocytes viability was detected by the MTT assay and Annexin V-FITC/PI dual staining assay. Caspase 3 activity was measured by using caspase 3 colorimetric assay kit. Apoptosis related proteins Bax, Bad, Bcl-xL, PCNA, p53 and phospho-p53, along with inflammation related protein MMP 3, MMP 9 and COX-2, and the expression of phospho-NF-kappaB p65 were assayed by western blotting analyses. Ro could improve IL-1beta-induced chondrocytes viability. Ro could suppress IL-1beta-induced apoptosis by inhibiting levels of Bax and Bad, decreasing p53 phosphorylation and promoting the expression of Bcl-xL and PCNA. Ro inhibited caspase 3 activity. IL-1beta-induced inflammation and matrix degration were also alleviated by Ro with down-regulating the expression of MMP 3, MMP 9 and COX-2. Moreover, Ro inhibited NF-kappaB p65 phosphorylation induced by IL-1beta. In conclusion, these results suggested Ro exerted anti-apoptosis and anti-inflammation in IL-1beta-induced rat chondrocytes, which might be related to NF-kappaB signal pathway. Therefore, we propose that Ro might be a potential novel drug for the treatment of osteoarthritis.

Anti-inflammatory activity of ginsenoside ro.[Pubmed:17221369]

Planta Med. 1990 Feb;56(1):19-23.

Ginsenoside Ro, an oleanane-type saponin has been screened for activity in experimental models of inflammation. Ginsenoside Ro (10,50, and 200 mg/kg, P. O.) inhibited an increase in vascular permeability in mice induced by acetic acid and reduced an acute paw edema in rats induced by compound 48/80 or carrageenin. Ginsenoside Ro did not suppress a developing adjuvant-induced edema in arthritic rats. However, Ginsenoside Ro was found to be effective in hypercoagulable state, increase of connective tissue in the artery and calcium effluence from the bone in adjuvant-induced arthritic rats.

Effects of ginseng rhizome and ginsenoside Ro on testosterone 5alpha-reductase and hair re-growth in testosterone-treated mice.[Pubmed:21538628]

Phytother Res. 2012 Jan;26(1):48-53.

This research program on the novel functions of Panax ginseng C. A. Meyer focused on the effects of ginseng rhizome on hair re-growth in androgenetic alopecia. Extracts of red ginseng rhizome showed greater dose-dependent inhibitory effects against testosterone 5alpha-reductase (5alphaR) when compared with extracts of the main root. Ginsenoside Ro, the predominant ginsenoside in the rhizome, and ginsenoside Rg(3), a unique ginsenoside in red ginseng, showed inhibitory activity against 5alphaR with IC(50) values of 259.4 and 86.1 microm, respectively. The rhizome of P. japonicus, which contains larger amounts of Ginsenoside Ro, also inhibited 5alphaR. Topical administration of extracts of red ginseng rhizomes (2 mg/mouse) and Ginsenoside Ro (0.2 mg/mouse) to shaved skin inhibited hair re-growth suppression after shaving in the testosterone-treated C57BL/6 mice. These results suggest that red ginseng rhizomes containing both oleanane- and dammarane-type ginsenosides are a promising raw material for cosmetic use. This is the first report that Ginsenoside Ro enhances in vivo hair re-growth based on their inhibitory activity against 5alphaR in the androgenetic alopecia model.

Antioxidative properties of ginsenoside Ro against UV-B-induced oxidative stress in human dermal fibroblasts.[Pubmed:26214051]

Biosci Biotechnol Biochem. 2015;79(12):2018-21.

Ginsenoside Ro (Ro), an oleanolic acid-type ginsenoside, exhibited suppressive activities on reactive oxygen species (ROS) and matrix metalloproteinase-2 (MMP-2) elevation in UV-B-irradiated fibroblasts. Ro could overcome the reduction of the total glutathione (GSH) contents in UV-B-irradiated fibroblasts. Ro could not interfere with cell viabilities in UV-B-irradiated fibroblasts. Collectively, Ro possesses a potential skin anti-photoaging property against UV-B radiation in fibroblasts.

Ginsenoside-Ro enhances cell proliferation and modulates Th1/Th2 cytokines production in murine splenocytes.[Pubmed:16011261]

Yao Xue Xue Bao. 2005 Apr;40(4):332-6.

AIM: To study the effects of ginsenoside-Ro on cell proliferation and cytokine production in murine splenocytes. METHODS: The effect of ginsenoside-Ro on murine splenocytes proliferation was studied using [3H] thymidine incorporation assay. Effects of ginsenoside-Ro on the production of cytokines interleukin-2 (IL-2), interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) from murine splenocytes were detected by ELISA method. Effects of ginsenoside-Ro on mRNA level of Th1 cytokine IFN-gamma and Th2 cytokine IL-4 were evaluated by reverse transcription polymerase chain reaction (RT-PCR) analysis. RESULTS: Ginsenoside-Ro showed no mitogenic effect on unstimulated murine splenocytes. It enhanced the proliferation of Con A-induced murine splenocytes and the production of IL-2 at concentrations of 1-10 micromol x L(-1). Moreover, ginsenoside-Ro increased the production and expression of Th2 cytokine IL-4 and decreased the production and expression of Th1 cytokine IFN-gamma in Con A-induced murine splenocytes at concentrations of 2-10 micromol x L(-1). CONCLUSION: Ginsenoside-Ro showed immunomodulatory effects by regulating the production and expression of Th1/Th2 cytokines in murine splenocytes.

Ginsenoside Ro (Polysciasaponin P3; Chikusetsusaponin 5; Chikusetsusaponin V) exhibits a Ca2+-antagonistic antiplatelet effect with an IC50 of 155 μM. Ginsenoside Ro reduces the production of TXA2 more than it reduces the activities of COX-1 and TXAS.

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