Ginsenoside Rb3

The roots of Panax ginseng C. A. Mey.

Ginsenoside Rb3 is extracted from steamed Panax notoginseng. Ginsenoside Rb3 exhibits inhibitory effect on TNFα-induced NF-κB transcriptional activity with an IC50 of 8.2 μM in 293T cell lines. Ginsenoside Rb3 also inhibits the induction of COX-2 and iNOS mRNA.

In Vitro:Ginsenoside Rb3 (0.1-10 μM) is tested for inhibition of tumor necrosis factor-α (TNF)-induced nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) luciferase reporter activity using a human kidney 293T cell-based assay. Ginsenoside Rb3 shows the significant activity with an IC50 of 8.2 μM. Ginsenoside Rb3 also inhibits the induction of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) messenger Ribonucleic acid (mRNA) in a dose-dependent manner after HepG2 cells have been treated with TNF-α (10 ng/mL)[1]. Ginsenoside Rb3 (0.1-10 μM) significantly increases cell viability and inhibits lactate dehydrogenase (LDH) release in a dose-dependent manner. PC12 cell viability as determined by MTT reduction is also markedly decreased after the cell is exposed to oxygen and glucose deprivation (OGD)/OGD-Rep. But, when the cells are pretreated with Ginsenoside Rb3 (0.1, 1, and 10 μM), OGD/OGD-Rep induced cell toxicity is significantly attenuated, which is concentration-dependently attenuated by Ginsenoside Rb3 treatment. The viabilities are raised to 52.8%±5.6%, 64.6%±5.7%, and 76.4%±8.8%, respectively, compared with the control group[2].

In Vivo:Ginsenosides Rb3 is a major compound isolated from Gynostemma pentaphyllum that holistically improves gut microenvironment and induces anti-polyposis in ApcMin/+ mice. Six-weeks-old mice are subjected to Rb3 treatment, before the appearance of the intestinal polyps. All the mice are monitored for food intake, water consumption, and weight changes. Throughout the experiment, no Rb3/Rd-associated weight loss in mice is observed. In addition, none of the treated mice show variations in food and water consumption. Whereas, the number and size of the polyps are effectively reduced by Rb3 treatments[3].

References:
[1]. He F, et al. Antitumor effects of dammarane-type saponins from steamed Notoginseng. Pharmacogn Mag. 2014 Jul;10(39):314-7. [2]. Zhu JR, et al. Protective effects of ginsenoside Rb(3) on oxygen and glucose deprivation-induced ischemic injury in PC12 cells. Acta Pharmacol Sin. 2010 Mar;31(3):273-80. [3]. Huang G, et al. Ginsenosides Rb3 and Rd reduce polyps formation while reinstate the dysbiotic gut microbiota and the intestinal microenvironment in ApcMin/+ mice. Sci Rep. 2017 Oct 2;7(1):12552.

Ginsenoside Rb3 exerts antidepressant-like effects in several animal models.[Pubmed:21948936]

J Psychopharmacol. 2012 May;26(5):697-713.

Total ginsenosides have been shown to have therapeutic actions as antidepressants. We report a major active ingredient of total ginsenosides, the Ginsenoside Rb3 (Rb3), which may have antidepressant-like effects. Using the forced swim test, tail suspension test, and learned helplessness procedure, we found that Rb3 had significant anti-immobility effects in mice in the forced swim and tail suspension tests and reduced the number of escape failures in the learned helplessness procedure. In a reserpine-induced syndrome model, Rb3 attenuated hypothermia, palpebral ptosis, and akinesia. In the chronic mild stress model, chronic Rb3 administration reversed the decrease in locomotor activity, novelty-suppressed feeding, and sucrose preference. Furthermore, neurochemical tests were performed to support our hypothesis that biochemical variations (i.e. brain-derived neurotrophic factor and the monoamine neurotransmitters 5-hydroxytryptamine, dopamine, and norepinephrine) are involved in Rb3's antidepressant-like effects. Finally, we found, using whole-cell patch-clamp recordings, that the action potential transmission in neurons within the somatosensory cortex was excited by Rb3 perfusion and blocked with Panax notoginseng total saponins extracted from leaves. This study provides evidence for the mechanism of action of the antidepressant-like effects of Rb3.

Ginsenoside Rb3 protects cardiomyocytes against ischemia-reperfusion injury via the inhibition of JNK-mediated NF-kappaB pathway: a mouse cardiomyocyte model.[Pubmed:25084093]

PLoS One. 2014 Aug 1;9(8):e103628.

Ginsenoside Rb3 is extracted from the plant Panax ginseng and plays important roles in cardiovascular diseases, including myocardial ischemia-reperfusion (I/R) injury. NF-kappaB is an important transcription factor involved in I/R injury. However, the underlying mechanism of Ginsenoside Rb3 in myocardial I/R injury remains poorly understood. In the current study, a model of myocardial I/R injury was induced via oxygen and glucose deprivation (OGD) followed by reperfusion (OGD-Rep) in mouse cardiac myoblast H9c2 cells. Our data demonstrate that Ginsenoside Rb3 suppresses OGD-Rep-induced cell apoptosis by the suppression of ROS generation. By detecting the NF-kappaB signaling pathway, we discover that the protective effect of Ginsenoside Rb3 on the OGD-Rep injury is closely related to the inhibition of NF-kappaB activity. Ginsenoside Rb3 inhibits the upregulation of phospho-IkappaB-alpha and nuclear translocation of NF-kappaB subunit p65 which are induced by ORD-Rep injury. In addition, the extract also inhibits the OGD-Rep-induced increase in the expression of inflammation-related factors, such as IL-6, TNF-alpha, monocyte chemotactic protein-1 (MCP-1), MMP-2 and MMP-9. However, LPS treatment alleviates the protective roles of Ginsenoside Rb3 and activates the NF-kappaB pathway. Finally, the upstream factors of NF-kappaB were analyzed, including the Akt/Foxo3a and MAPK signaling pathways. We find that Ginsenoside Rb3 pretreatment only decreases the phosphorylation of JNK induced by OGD-Rep injury, an indicator of the MAPK pathway. Importantly, an inhibitor of phospho-JNK, SP600125, protects against OGD-Rep induced apoptosis and inhibited NF-kappaB signaling pathway, similar to the roles of Ginsenoside Rb3. Taken together, our results demonstrate that the protective effect of Ginsenoside Rb3 on the OGD-Rep injury is attributed to the inhibition of JNK-mediated NF-kappaB activation, suggesting that Ginsenoside Rb3 has the potential to serve as a novel therapeutic agent for myocardial I/R injury.

Anti-diabetic effect of ginsenoside Rb(3) in alloxan-induced diabetic mice.[Pubmed:22741793]

Med Chem. 2012 Sep;8(5):934-41.

As one of the main active component of protopanaxdiol type ginsenosides, ginsenoside Rb(3) is rarely reported in the treatment of diabetes. The anti-diabetic activity of ginsenoside Rb(3) was investigated in a model of alloxan-induced diabetic mice in the present study. The physiological parameter such as fasting blood glucose level, oral glucose tolerance, body weight, food intake and water intake were measured. Glucose consumption in C2C12 myotubes was also determined in order to investigate the molecular mechanism of ginsenoside Rb(3) in anti-diabetes. The alloxan-induced diabetic mice were treated with ginsenoside Rb(3) for 2 weeks at doses of 5 mg/kg, 15 mg/kg and 25 mg/kg. After 2 weeks treatment of ginsenoside Rb(3), the fasting blood glucose levels of DG 15 and DG 25 were respectively reduced by 36.70% and 37.50% compared to control group. At a dose of 25 mg/kg, oral glucose tolerance was significantly improved compared to control group (P < 0.05). The AUC decreased by 34.47% (from 2442 +/- 291 mmol.min/L to 1600 +/- 109 mmol.min/L). Both food intake and water intake were remarkably lowered. The injury of pancreas tissues was repaired, which was observed by using HE staining and optic microscope. In vitro, at concentrations of 100 and 200 microM, ginsenoside Rb(3) increased glucose consumption in C2C12 myotubes by 76.83% and 97.20%, respectively, as compared to the control group. However, the body weight of diabetic mice was not significantly altered. In conclusion, our results showed that ginsenoside Rb(3) reduced fasting blood glucose level, food intake, water intake, improved oral glucose tolerance, and repaired injured pancreas tissues of alloxan-induced diabetic mice. Therefore, it was suggested that ginsenoside possesses the potential of the clinical use in preventing and treating diabetes.

[The estrogen-like protective effect of ginsenoside Rb3 on oxidative stress and dysfunction of endothelial cells induced by oxidized low-density lipoprotein].[Pubmed:25577870]

Yao Xue Xue Bao. 2014 Oct;49(10):1406-12.

Ginsenoside Rb3 (GRb3) is one of the main components in plasma of Panax quinquefolius Saponin of stem and leaf (PQS), which can be into human plasma. Previous studies have found PQS has estrogen-like vascular protective effects. In the present study, we investigated the estrogen-like protective effect of GRb3 on oxidative stress and dysfunction of endothelial cells induced by oxidized low-density lipoprotein. The activities of SOD, NOS and the contents of MDA in the cell lysate were examined by enzyme method or spectrophotometry. The NO and ET-1 concentrations in the cell culture supernatant were measured by ELISA method. The iNOS and eNOS mRNA expression were measured by real time RT-PCR, while the phosphorylation levels of Akt was measured by Western blotting. The results showed that GRb3 could enhance the activity of SOD, reduce the content of MDA, increase the level of NOS, NO, ET-1 and iNOS mRNA expression while decrease the eNOS mRNA expression and the phosphorylation level of Akt. These effects were blocked by estrogen receptor antagonist ICI182780. GRb3 can play a role in protecting vascular endothelial cells by estrogen receptors, the protective mechanism is similar to 17-beta estrodiol.

Ginsenoside Rb3 attenuates oxidative stress and preserves endothelial function in renal arteries from hypertensive rats.[Pubmed:24571453]

Br J Pharmacol. 2014 Jul;171(13):3171-81.

BACKGROUND AND PURPOSE: Panax ginseng is commonly used to treat cardiovascular conditions in Oriental countries. This study investigated the mechanisms underlying the vascular benefits of Ginsenoside Rb3 (Rb3) in hypertension. EXPERIMENTAL APPROACH: Rings of renal arteries were prepared from spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats and were cultured ex vivo for 8 h. Contractile responses of the rings were assessed with myograph techniques. Expression of NADPH oxidases was assessed by Western blotting and immunohistochemistry. Reactive oxygen species (ROS) were measured using dihydroethidium fluorescence imaging and production of NO was determined using the fluorescent NO indicator DAF-FM diacetate in human umbilical vein endothelial cells. KEY RESULTS: Ex vivo treatment with Rb3 concentration-dependently augmented endothelium-dependent relaxations, suppressed endothelium-dependent contractions and reduced ROS production and expressions of NOX-2, NOX-4 and p67(phox) in arterial rings from SHR. Rb3 treatment also normalized angiotensin II (Ang II)-stimulated elevation in ROS and expression of NOX-2 and NOX-4 in arterial rings from WKY rats. Rb3 inhibited Ang II-induced reduction of NO production and phosphorylation of endothelial NOS in cultures of human umbilical vein endothelial cells. Rb3 also inhibited oxidative stress in renal arterial rings from hypertensive patients or in Ang II-treated arterial rings from normotensive subjects. CONCLUSION AND IMPLICATIONS: Ex vivo Rb3 treatment restored impaired endothelial function in arterial rings from hypertensives by reversing over-expression of NADPH oxidases and over-production of ROS, and improved NO bioavailability. Our findings suggest that medicinal plants containing Rb3 could decrease oxidative stress and protect endothelial function in hypertension.

Inhibition of NMDA receptors underlies the neuroprotective effect of ginsenoside Rb3.[Pubmed:19655413]

Am J Chin Med. 2009;37(4):759-70.

In order to investigate the mechanisms underlying the neuroprotective effect of Ginsenoside Rb3, rat hippocampal neurons were primarily cultured, and exposed to 1 mM N-methyl-D-aspartate (NMDA), cell viability and lactate dehydrogenase leakage were measured. Ca2+ influx was determined by calcium imaging with a laser confocal microscopy. The influences of Ginsenoside Rb3 on these variables were examined. Patch-clamp technique was used to observe the effects of Ginsenoside Rb3 on NMDA-evoked current. The results show that treatment of Rb3 raised the neuronal viability, reduced the leakage of lactate dehydrogenase, and inhibited NMDA-elicited Ca2+ influx in a dose-dependent manner. In the presence of Rb3, NMDA-evoked peak current was inhibited, and Ca2+-induced desensitization of NMDA current was facilitated. It is suggested that Ginsenoside Rb3 could exert a neuroprotective role on hippocampal neurons, a role which was partly mediated by the facilitation of Ca2+-dependent deactivation of NMDA receptors, and the resultant reduction of intracellular free Ca2+ level.

Ginsenoside-Rb3 protects the myocardium from ischemia-reperfusion injury via the inhibition of apoptosis in rats.[Pubmed:25371727]

Exp Ther Med. 2014 Dec;8(6):1751-1756.

Ginsenoside-Rb3 (G-Rb3) has been previously demonstrated to attenuate myocardial ischemia-reperfusion injury (MIRI). The aim of the present study was to investigate this further and determine whether G-Rb3 protects the myocardium from ischemia-reperfusion injury via the inhibition of apoptosis. Adult male Sprague Dawley rats were randomly divided into four groups: Sham, MIRI, G-Rb3 treatment (orally, 20 mg/kg) and ischemic postconditioning (as the positive control). The drug or placebo treatment was administered to the rats once a day for three consecutive days, and MIRI was then induced by subjecting the rats to left anterior descending coronary artery ligation for 30 min and reperfusion for 2 h. The results showed that G-Rb3 treatment significantly reduced the number of apoptotic cells in the myocardium and the expression of B-cell lymphoma 2-associated X protein, and increased the expression of B-cell lymphoma 2. The activities of aspartate aminotransferase, lactate dehydrogenase and creatine kinase-MB in the serum were also reduced significantly by the G-Rb3 treatment. These findings suggest that G-Rb3 inhibits apoptosis in the early stage of MIRI, and attenuates MIRI when the reperfusion continues. G-Rb3 was also shown to significantly reduce the level of malondialdehyde and increase the activity of superoxide dismutase in the myocardium, which suggests that attenuating reactive oxygen species accumulation and oxidative stress may be the major mechanism underlying the anti-apoptotic effects of G-Rb3. The release of inflammatory factors was significantly attenuated by G-Rb3, which may also be associated with its anti-apoptotic effects.

Ginsenoside Rb3 is extracted from steamed Panax notoginseng. Ginsenoside Rb3 exhibits inhibitory effect on TNFα-induced NF-κB transcriptional activity with an IC50 of 8.2 μM in 293T cell lines. Ginsenoside Rb3 also inhibits the induction of COX-2 and iNOS mRNA.

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