White crystalline powder
Panax ginseng C. A. Mey./Panax ginseng
(3β,12β,20Z)-12-Hydroxydammara-20(22),24-dien-3-yl β-D-glucopyranoside/β-D-Glucopyranoside, (3β,12β,20Z)-12-hydroxydammara-20(22),24-dien-3-yl/GinsenosideRh3/N1608/Ginsenoside Rh3
Ginsenoside Rh3 is a bacterial metabolite of Ginsenoside Rg5. Ginsenoside Rh3 treatment in human retinal cells induces Nrf2 activation
Soluble ≥5 mg/ml in DMSO
695.0±55.0 °C at 760 mmHg
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For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:105558-26-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Four representative Δ20-ginsenosides, namely, ginsenosides Rh4 (1), (20E)-Rh3 (2), Rg6 (3), and Rk1 (4) from Panax Ginseng, were chemically synthesized for the first time. Dehydration of the naturally occurring 20(S)-protopanaxatriol and 20(S)-protopanaxadiol provided all types of Δ20-sapogenins, which were separated due to a judicious choice of protecting groups. The Δ20-sapogenins were then directly glycosylated with glycosyl ortho-alkynylbenzoate donors under the catalysis of Ph3PAuNTf2 as key steps. The neutral conditions of the glycosylations were crucial to prevent the acid-labile Δ20,21 double bond from isomerization.
Synthesis of Δ20-Ginsenosides Rh4, (20E)-Rh3, Rg6, and Rk1: A General Approach To Access Dehydrated Ginsenosides.
Shen R1, Laval S1, Cao X1, Yu B1.
2018 Mar 2;83
Excessive Ultra-violet (UV) radiation shall induce damages to resident retinal pigment epithelium (RPE) cells (RPEs) and retinal ganglion cells (RGCs). Here we tested the potential activity of Ginsenoside Rh3 (“Rh3”) against the process. In cultured human RPEs and RGCs, pretreatment with Rh3 inhibited UV-induced reactive oxygen species (ROS) production and following apoptotic/non-apoptotic cell death. Rh3 treatment in retinal cells induced nuclear-factor-E2-related factor 2 (Nrf2) activation, which was evidenced by Nrf2 protein stabilization and its nuclear translocation, along with transcription of antioxidant responsive element (ARE)-dependent genes (HO1, NOQ1 and GCLC). Nrf2 knockdown by targeted-shRNA almost abolished Rh3-induced retinal cell protection against UV. Further studies found that Rh3 induced microRNA-141 (“miR-141”) expression, causing downregulation of its targeted gene Keap1 in RPEs and RGCs. On the other hand, Rh3-induced Nrf2 activation and retinal cell protection were largely attenuated by the miR-141’s inhibitor, antagomiR-141. In vivo, intravitreal injection of Rh3 inhibited retinal dysfunction by light damage in mice. Rh3 intravitreal injection also induced miR-141 expression, Keap1 downregulation and Nrf2 activation in mouse retinas. We conclude that Rh3 protects retinal cells from UV via activating Nrf2 signaling.
Copyright © 2018 Elsevier Inc. All rights reserved.
Ginsenoside Rh3; MicroRNA-141; Nrf2, UV radiation; Oxidative stress; Retinal cells
Activation of Nrf2 by Ginsenoside Rh3 protects retinal pigment epithelium cells and retinal ganglion cells from UV.
Tang CZ1, Li KR2, Yu Q2, Jiang Q3, Yao J4, Cao C5.
Ginsenoside Rh3 is a bacterial metabolite of Rg5, which is the main constituent of heat-processed ginseng. The present study was undertaken to examine the anti-inflammatory effect of ginsenoside Rh3 in lipopolysaccharide (LPS)-stimulated microglia. Rh3 inhibits the expressions of inducible nitric oxide synthase (iNOS) and proinflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, at mRNA and protein levels, while Rh3 enhanced anti-inflammatory hemeoxygenase-1 expression. Moreover, Rh3 inhibited nuclear factor-κB (NF-κB) by upregulation of sirtuin 1 (SIRT1) and enhanced Nrf2 DNA-binding activities. Analysis of signaling pathways revealed that Rh3 enhanced the phosphorylation of 5′-adenosine monophosphate-activated protein kinase (AMPK) and inhibited Akt and janus kinase 1 (JAK1)/signal transducer and activator of transcription 1 (STAT1) induced by LPS. By treatment of BV2 cells with AICAR (a pharmacological activator of AMPK), we found that AMPK is an upstream regulator of phosphatidylinositol 3-kinase (PI3K)/Akt and JAK1/STAT1. Furthermore, AMPK knockdown experiments demonstrated the anti-inflammatory role of AMPK in LPS/Rh3-treated BV2 microglia. Our data collectively suggest that Rh3 exerts an anti-inflammatory effect in microglia by modulating AMPK and its downstream signaling pathways.
AMPK; ginsenoside Rh3; microglia; neuroinflammation; signaling molecules
Anti-inflammatory mechanism of ginseng saponin metabolite Rh3 in lipopolysaccharide-stimulated microglia: critical role of 5'-adenosine monophosphate-activated protein kinase signaling pathway.
Lee YY, Park JS, Lee EJ, Lee SY1, Kim DH1, Kang JL, Kim HS.
2015 Apr 8