| Description: |
Ginsenoside Rb1 is a protopanaxadiol that has diverse in vitro and in vivo effects, including neuroprotective, cardioprotective, anti-obesity, anti-inflammatory, and anti-oxidative actions. Ginsenoside Rb1 can up-regulate the expression of GLUTs in adipose tissue, in addition to activate insulin signalling pathway, and may effectively ameliorate the progression of asthma through Relegating Th1/Th2. It inhibited Na+, K+-ATPase activity with an IC50 of 6.3±1.0 μM, activated Akt, phosphorylating GSK-3β and inhibited mPTP opening. |
| Targets: |
p38MAPK | JNK | GLUT | Akt | IFN-γ | IL Receptor | GSK-3 | HO-1 | PKA | Estrogen receptor | Progestogen receptor |
| In vitro: |
| Zhongguo Yao Li Xue Bao . 1990 Jan;11(1):10-4. | | Inhibitory effects of ginsenoside Rg1 and Rb1 on rat brain microsomal Na+,K(+)-ATPase activity[Pubmed: 2169691] | | Rat brain microsomal Na+, K(+)-ATPase activity was inhibited significantly and rapidly by ginsenoside Rb1. The IC50 of Rb1 for Na+,K(+)-ATPase was 6.3 +/- 1.0 mumol/L. The inhibition was enhanced with increasing the concentration of Rb1 or decreasing that of Na+ and K+. Kinetic analysis revealed that ginsenoside was an uncompetitive inhibitor with respect to ATP. The inhibitory effect of Rg1 on rat brain microsomal Na+,K(+)-ATPase was much weaker than that of Rb1. | | Drug Metab Dispos . 2015 Aug;43(8):1181-9. | | Ginsenosides Regulate PXR/NF-κB Signaling and Attenuate Dextran Sulfate Sodium-Induced Colitis[Pubmed: 25986850] | | Pregnane X receptor (PXR) activation exhibits anti-inflammatory effects via repressing nuclear factor-κB (NF-κB); however, its overactivation may disrupt homeostasis of various enzymes and transporters. Here we found that ginsenosides restore PXR/NF-κB signaling in inflamed conditions without disrupting PXR function in normal conditions. The effects and mechanisms of ginsenosides in regulating PXR/NF-κB signals were determined both in vitro and in vivo. Ginsenosides significantly inhibited NF-κB activation and restored the expression of PXR target genes in tumor necrosis factor-α-stimulated LS174T cells. Despite not being PXR agonists, ginsenosides repressed NF-κB activation in a PXR-dependent manner. Ginsenosides significantly increased the physical association between PXR and the NF-κB p65 subunit and thereby decreased the nuclear translocation of p65. Ginsenoside Rb1 and compound K (CK) were major bioactive compounds in the regulating PXR/NF-κB signaling. Consistently, ginsenosides significantly attenuated dextran sulfate sodium-induced experimental colitis, which was associated with restored PXR/NF-κB signaling. This study indicates that ginsenosides may elicit anti-inflammatory effects via targeting PXR/NF-κB interaction without disrupting PXR function in healthy conditions. Ginsenoside Rb1 and CK may serve as leading compounds in the discovery of new drugs that target PXR/NF-κB interaction in therapy for inflammatory bowel disease. | | Biochem Pharmacol . 2011 Aug 1;82(3):278-86. | | Ginsenoside Rb1 and its metabolite compound K inhibit IRAK-1 activation--the key step of inflammation[Pubmed: 21600888] | | In the preliminary study, ginsenoside Rb1, a main constituent of the root of Panax ginseng (family Araliaceae), and its metabolite compound K inhibited a key factor of inflammation, nuclear transcription factor κB (NF-κB) activation, in lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages. When ginsenoside Rb1 or compound K were orally administered to 2,4,6-trinitrobenzene sulfuric acid (TNBS)-induced colitic mice, these agents inhibited colon shortening, macroscopic score, and colonic thickening. Furthermore, treatment with ginsenoside Rb1 or compound K at 20mg/kg inhibited colonic myeloperoxidase activity by 84% and 88%, respectively, as compared with TNBS alone (p<0.05), and also potently inhibited the expression of tumor necrosis factor-α, interleukin (IL)-1β and IL-6, but increased the expression of IL-10. Both ginsenoside Rb1 and compound K blocked the TNBS-induced expressions of COX-2 and iNOS and the activation of NF-κB in mice. When ginsenoside Rb1 or compound K was treated in LPS-induced murine peritoneal macrophages, these agents potently inhibited the expression of the proinflammatory cytokines. Ginsenoside Rb1 and compound K also significantly inhibited the activation of interleukin-1 receptor-associated kinase-1 (IRAK-1), IKK-β, NF-κB, and MAP kinases (ERK, JNK, and p-38); however, interaction between LPS and Toll-like receptor-4, IRAK-4 activation and IRAK-2 activation were unaffected. Furthermore, compound K inhibited the production of proinflammatory cytokines more potently than did those of ginsenoside Rb1. On the basis of these findings, ginsenosides, particularly compounds K, could be used to treat inflammatory diseases, such as colitis, by targeting IRAK-1 activation. |
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| In vivo: |
| Vascul Pharmacol. 2015 Oct;73:86-95. | | Ginsenoside Rb1 attenuates angiotensin II-induced abdominal aortic aneurysm through inactivation of the JNK and p38 signaling pathways.[Pubmed: 25912763] | Abdominal aortic aneurysm (AAA), a life-threatening vascular disease, accounts for approximately 10% of the morbidity in people over 65years old. No satisfactory approach is available to treat AAA. Ginsenosides Rb1 and Rg1 are primary ingredients of Panax notoginseng for the treatment of cardiovascular diseases, but their impact on AAA is unknown.
METHODS AND RESULTS:
An AAA model was established using an Ang II infusion in ApoE-/- mice. After continuous stimulation of Ang II for 28days, suprarenal aortic aneurysms developed in 77% mice and 12% mice died suddenly due to AAA rupture. Administration of Ginsenoside Rb1 (20mg/kg/day), but not ginsenoside Rg1, significantly reduced the incidence and mortality of AAA. Ginsenoside Rb1 treatment dramatically suppressed Ang II-induced diameter enlargement, extracellular matrix degradation, matrix metalloproteinase (MMP) production, inflammatory cell infiltration, and vascular smooth muscle cell (VSMC) dysfunction. Mechanistic studies indicated that the protective effects of Ginsenoside Rb1 were associated with the inactivation of JNK and p38 MAPK signaling pathways. A specific activator of JNK and p38, anisomycin, nearly abolished Ginsenoside Rb1-driven suppression of MMP secretion by VSMCs.
CONCLUSIONS:
Ginsenoside Rb1, as a potential anti-AAA agent, suppressed AAA through inhibiting the JNK and p38 signaling pathways. | | Inflammation. 2015 Oct;38(5):1814-22. | | Anti-Asthmatic Effects of Ginsenoside Rb1 in a Mouse Model of Allergic Asthma Through Relegating Th1/Th2.[Pubmed: 25832478] | The aim of the study was to investigate the anti-asthma effects of ginsenoside Rb1 (Rb1) and its possible mechanisms.
METHODS AND RESULTS:
A total of 50 mice were randomly assigned to five experimental groups: control, model, dexamethasone (2 mg/kg), and Rb1 (10 and 20 mg/kg). Airway resistance (RI) was measured; histological studies were evaluated by the hematoxylin and eosin (HE) staining; Th1/Th2, ovalbumin (OVA)-specific serum, and bronchoalveolar lavage fluid (BALF) IgE levels were evaluated enzyme-linked immunosorbent assay (ELISA); and T-bet/GATA3 proteins were evaluated by Western blot. Our study demonstrated that Rb1 inhibited OVA-induced increases in RI and eosinophil counts; interleukin (IL)-4 was recovered, and IFN-γlevel increased in bronchoalveolar lavage fluid. Histological studies demonstrated that Rb1 substantially inhibited OVA-induced eosinophilia in lung tissue. Western blot studies demonstrated that Rb1 substantially inhibited GATA3 and increased T-bet.
CONCLUSIONS:
These findings suggest that Rb1 may effectively ameliorate the progression of asthma and could be used as a therapy for patients with allergic asthma. | | Pharmacogn Mag. 2014 Oct;10(40):458-63. | | Effects of ginsenosides-Rb1 on exercise-induced oxidative stress in forced swimming mice.[Pubmed: 25422546] | The fleshy root of Panax ginseng C.A. Meyer (ginseng) is one of the most well-known and valued herbs in traditional Chinese medicine. Ginsenosides are considered mainly responsible for the pharmacological activities of ginseng. The purpose of this study was to investigate the effects of ginsenoside-Rb1 (G-Rb1) on swimming exercise-induced oxidative stress in male mice.
METHODS AND RESULTS:
A total of 48 animals were randomly divided into four groups, with twelve mice in each group. The first, second and third groups were designed as G-Rb1 treatment groups, got 25, 50 and 100 mg/kg bodyweight of G-Rb1, respectively. The fourth group was designed as the control group, got physiologic saline. The mice were intragastrically administered once daily for 4 weeks. The weight-loaded forced swimming test was conducted on the final day of experimentation. Then the exhaustive swimming time, blood lactate, serum creatine kinase (CK), malondialdehyde (MDA) and antioxidant enzymes in liver of mice were measured.
The results showed that G-Rb1 could prolong the exhaustive swimming time and improve exercise endurance capacity of mice, as well as accelerate the clearance of blood lactate and decrease serum CK activities. Meanwhile, G-Rb1 could decrease MDA contents and increase superoxide dismutase, catalase, glutathione peroxidase activities in liver of mice.
CONCLUSIONS:
The study suggested that G-Rb1 possessed protective effects on swimming exercise-induced oxidative stress in mice. |
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