| Description: |
Ginsenoside Rb2 shows hypoglycemic, anti-osteoporosis, anti-oxidant, anti-angiogenesis, and anti-tumor activities, it is a promising candidate as a mucosal immunoadjuvant to enhance antiviral activity and is a valuable component capable of lowering the levels of lipids. Ginsenoside Rb2 also possesses a protective role against the photoaging of human keratinocyte cells under UV-B irradiation, shows inhibitory effects on nicotinic stimulation-evoked catecholamine secretion, at least partly through the increased NO production due to the activation of nitric oxide synthase, which is relevant to neuronal nicotinic receptor blockade.
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| In vitro: |
| Biosci Biotechnol Biochem. 2015 Mar 16:1-7. | | Suppressive properties of ginsenoside Rb2, a protopanaxadiol-type ginseng saponin, on reactive oxygen species and matrix metalloproteinase-2 in UV-B-irradiated human dermal keratinocytes.[Pubmed: 25774540] | Ginsenosides, also known as ginseng saponins, are the principal bioactive ingredients of ginseng, which are responsible for its diverse pharmacological activities. The present work aimed to assess skin anti-photoaging properties of ginsenoside Rb2 (Rb2), one of the predominant protopanaxadiol-type ginsenosides, in human epidermal keratinocyte HaCaT cells under UV-B irradiation.
METHODS AND RESULTS:
When the cultured keratinocytes were subjected to Rb2 prior to UV-B irradiation, Rb2 displayed suppressive activities on UV-B-induced reactive oxygen species elevation and matrix metalloproteinase-2 expression and secretion. However, Rb2 at the used concentrations was unable to modulate cellular survivals in the UV-B-irradiated keratinocytes.
CONCLUSIONS:
In brief, Rb2 possesses a protective role against the photoaging of human keratinocyte cells under UV-B irradiation. | | Korean J Physiol Pharmacol. 2014 Oct;18(5):431-9. | | Inhibitory effects of ginsenoside-rb2 on nicotinic stimulation-evoked catecholamine secretion.[Pubmed: 25352764] | The aim of the present study was to investigate whether ginsenoside Rb2 (Rb2) can affect the secretion of catecholamines (CA) in the perfused model of the rat adrenal medulla.
METHODS AND RESULTS:
Rb2 (3~30 μM), perfused into an adrenal vein for 90 min, inhibited ACh (5.32 mM)-evoked CA secretory response in a dose- and time-dependent fashion. Rb2 (10 μM) also time-dependently inhibited the CA secretion evoked by DMPP (100 μM, a selective neuronal nicotinic receptor agonist) and high K(+) (56 mM, a direct membrane depolarizer). Rb2 itself did not affect basal CA secretion (data not shown). Also, in the presence of Rb2 (50 μg/mL), the secretory responses of CA evoked by veratridine (a selective Na(+) channel activator (50 μM), Bay-K-8644 (an L-type dihydropyridine Ca(2+) channel activator, 10 μM), and cyclopiazonic acid (a cytoplasmic Ca(2+)-ATPase inhibitor, 10 μM) were significantly reduced, respectively. Interestingly, in the simultaneous presence of Rb2 (10 μM) and L-NAME (an inhibitor of NO synthase, 30 μM), the inhibitory responses of Rb2 on ACh-evoked CA secretory response was considerably recovered to the extent of the corresponding control secretion compared with the inhibitory effect of Rb2-treatment alone. Practically, the level of NO released from adrenal medulla after the treatment of Rb2 (10 μM) was greatly elevated compared to the corresponding basal released level.
CONCLUSIONS:
Collectively, these results demonstrate that Rb2 inhibits the CA secretory responses evoked by nicotinic stimulation as well as by direct membrane-depolarization from the isolated perfused rat adrenal medulla. It seems that this inhibitory effect of Rb2 is mediated by inhibiting both the influx of Ca(2+) and Na(+) into the adrenomedullary chromaffin cells and also by suppressing the release of Ca(2+) from the cytoplasmic calcium store, at least partly through the increased NO production due to the activation of nitric oxide synthase, which is relevant to neuronal nicotinic receptor blockade. | | 2017 Feb;38(2):192-200. | | Ginsenoside Rb2 enhances the anti-inflammatory effect of ω-3 fatty acid in LPS-stimulated RAW264.7 macrophages by upregulating GPR120 expression[Pubmed: 28017961] | | Recent studies confirm that chronic low-grade inflammation is closely associated with metabolic syndromes, and anti-inflammatory therapy is a potential approach for treating cardiovascular diseases and type 2 diabetes. Accumulating evidence suggests that GPR120 activation is a feasible solution to ameliorating chronic inflammation and improving glucose metabolism. In this study we investigated whether ginsenoside Rb2 (Rb2), which exhibited regulatory activities in glucose and lipid metabolism, affected GPR120 expression in lipopolysaccharide (LPS)-activated mouse macrophage RAW264.7 cells, and examined the contribution of GPR120 activation to reducing the LPS-induced inflammatory response. LPS (100 ng/mL) activated the macrophages, resulting in dramatic increases in TNF-α, IL-6, IL-1β and NO production. Treatment with a ω-3 fatty acid α-linolenic acid (ALA, 50 μmol/L) produced moderate reduction in LPS-stimulated inflammatory cytokines and NO production (TNF-α and IL-6 were decreased by 46% and 42%, respectively). Pre-incubation with Rb2 (1 or 10 μmol/L) for 12 h before ALA treatment dramatically amplified the inhibitory effects of ALA (TNF-α and IL-6 were decreased by 74% and 86%, respectively). Compared to the treatment with ALA alone, pre-incubation with Rb2 resulted in a more prominent reduction in LPS-stimulated expression of iNOS and COX-2 and LPS-stimulated IKK/NF-κB phosphorylation and MAPK pathway activation. Rb2 (0.1-100 μmol/L) dose- and time-dependently increased both mRNA and protein expression of GPR120 in RAW264.7 cells, but treatment with Rb2 alone did not exert anti-inflammatory effect in LPS-activated RAW264.7 cells. In RAW264.7 cells transfected with GPR120 shRNA, the ameliorating effects of Rb2 on LPS-induced inflammation were abolished. In conclusion, Rb2 exerts anti-inflammatory effect in LPS-stimulated mouse macrophage RAW264.7 cells in vitro by increasing GPR120 expression and subsequently enhancing ω-3 fatty acid-induced GPR120 activation. |
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| In vivo: |
| Biol Pharm Bull. 1994 May;17(5):635-9. | | Inhibition of tumor angiogenesis and metastasis by a saponin of Panax ginseng, ginsenoside-Rb2.[Pubmed: 7522731] | We studied the effect of ginsenoside Rb2 extracted from Panax ginseng on angiogenesis and metastasis produced by B16-BL6 melanoma cells in syngeneic mice.
METHODS AND RESULTS:
Intravenous administration of ginsenoside Rb2 on day 1, 3 or 7 after tumor inoculation achieved a remarkable reduction in the number of vessels oriented toward the tumor mass, but did not cause a significant inhibition of tumor growth. The anti-angiogenic effect was dose-dependent ranging from 10 to 500 micrograms/mouse. In contrast, intra-tumoral or oral administration of ginsenoside Rb2 caused a marked inhibition of both neovascularization and tumor growth. Ginsenoside Rb2 did not affect the growth of rat lung endothelial (RLE) cells, B16-BL6 melanoma cells or various types of murine normal cells in vitro. The invasion of RLE cells into the reconstituted basement membrane (Matrigel), which is considered to be an essential event in tumor neovascularization, was inhibited by ginsenoside Rb2 in a concentration-dependent fashion, while ginsenoside Rb2 did not inhibit the haptotactic migration of endothelial cells to fibronectin-substrate. Multiple administrations of ginsenoside Rb2 after the intravenous inoculation of B16-BL6 melanoma cells resulted in a significant inhibition of lung metastasis as compared with the untreated control.
CONCLUSIONS:
These results suggest that the inhibition of tumor-associated angiogenesis by ginsenoside Rb2 may partly contribute to the inhibition of lung tumor metastasis. |
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