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Ruscogenin

$178

  • Brand : BIOFRON

  • Catalogue Number : BF-R2003

  • Specification : 98%

  • CAS number : 472-11-7

  • Formula : C27H42O4

  • Molecular Weight : 430.62

  • PUBCHEM ID : 441893

  • Volume : 20mg

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Catalogue Number

BF-R2003

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

430.62

Appearance

White crystal

Botanical Source

root of Ophiopogon japonicus

Structure Type

Others

Category

Standards;Natural Pytochemical;API

SMILES

CC1CCC2(C(C3C(O2)CC4C3(CCC5C4CC=C6C5(C(CC(C6)O)O)C)C)C)OC1

Synonyms

(1β,3β,25R)-Spirost-5-ene-1,3-diol/25D-Spirost-5-ene-1|A,3|A-diol/(25R)-Spirost-5-ene-1b,3b-diol/(25R)-Spirost-5-ene-1β,3β-diol/(1β,3β,25R)-Spirost-5-en-1,3-diol/Spirost-5-en-1,3-diol, (1β,3β,25R)-

IUPAC Name

(1S,2S,4S,5'R,6R,7S,8R,9S,12S,13R,14R,16R)-5',7,9,13-tetramethylspiro[5-oxapentacyclo[10.8.0.02,9.04,8.013,18]icos-18-ene-6,2'-oxane]-14,16-diol

Density

1.2±0.1 g/cm3

Solubility

Methanol; Acetone

Flash Point

294.4±30.1 °C

Boiling Point

563.1±50.0 °C at 760 mmHg

Melting Point

198-202ºC

InChl

InChI=1S/C27H42O4/c1-15-7-10-27(30-14-15)16(2)24-22(31-27)13-21-19-6-5-17-11-18(28)12-23(29)26(17,4)20(19)8-9-25(21,24)3/h5,15-16,18-24,28-29H,6-14H2,1-4H3/t15-,16+,18-,19-,20+,21+,22+,23-,24+,25+,26+,27-/m1/s1

InChl Key

QMQIQBOGXYYATH-IDABPMKMSA-N

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:472-11-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

27589720

Abstract

Ruscogenin, an important steroid sapogenin derived from Ophiopogon japonicus, has been shown to inhibit cerebral ischemic injury. However, its potential molecular action on blood-brain barrier (BBB) dysfunction after stroke remains unclear. This study aimed to investigate the effects of ruscogenin on BBB dysfunction and the underlying mechanisms in middle cerebral artery occlusion/reperfusion (MCAO/R)-injured mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-injured mouse brain microvascular endothelial cells (bEnd.3). The results demonstrated that administration of ruscogenin (10 mg/kg) decreased the brain infarction and edema, improved neurological deficits, increased cerebral brain flow (CBF), ameliorated histopathological damage, reduced evans blue (EB) leakage and upregulated the expression of tight junctions (TJs) in MCAO/R-injured mice. Meanwhile, ruscogenin (0.1-10 µM) treatment increased cell viability and trans-endothelial electrical resistance (TEER) value, decreased sodium fluorescein leakage, and modulated the TJs expression in OGD/R-induced bEnd.3 cells. Moreover, ruscogenin also inhibited the expression of interleukin-1β (IL-1β) and caspase-1, and markedly suppressed the expression of Nucleotide-binding domain (NOD)-like receptor family, pyrin domain containing 3 (NLRP3) and thiredoxin-interactive protein (TXNIP) in vivo and in vitro. Furthermore, ruscogenin decreased reactive oxygen species (ROS) generation and inhibited the mitogen-activated protein kinase (MAPK) pathway in OGD/R-induced bEnd.3 cells. Our findings provide some new insights into its potential application for the prevention and treatment of ischemic stroke.

KEYWORDS

MAPK; blood-brain barrier; inflammasome; ischemic stroke; ruscogenin.

Title

Ruscogenin Attenuates Cerebral Ischemia-Induced Blood-Brain Barrier Dysfunction by Suppressing TXNIP/NLRP3 Inflammasome Activation and the MAPK Pathway

Author

Guosheng Cao 1 , Nan Jiang 2 , Yang Hu 3 , Yuanyuan Zhang 4 , Guangyun Wang 5 , Mingzhu Yin 6 , Xiaonan Ma 7 , Kecheng Zhou 8 , Jin Qi 9 , Boyang Yu 10 , Junping Kou 11

Publish date

2016 Aug 29

PMID

29477471

Abstract

Background: Hepatocellular carcinoma (HCC) is the third-leading cause of cancer-related mortality with poor prognosis and treatment. More effective strategies should be studied in HCC.
Methods: After treated with ruscogenin, the cell proliferation was assessed by CCK-8 method. Cell migration and invasion were estimated using wound healing and transwell assays. Pathological changes of lung tissue were observed by HE staining and IHC methods. MMP-2, MMP-9, uPA, VEGF and HIF-1α levels were measured using ELISA, RT-qPCR and WB tests. PI3K/Akt/mTOR pathway related molecules were detected using WB analysis.
Results: The results indicated the hypotoxicity of ruscogenin. Meanwhile, ruscogenin showed obvious interruption on the cancer cell migration and invasion, and inhibition on the metastatic foci in pulmonary tissue. Significantly, ruscogenin decreased the levels of MMP-2, MMP-9, uPA, VEGF and HIF-1α, down-regulated the phosphorylation of Akt, mTOR.
Conclusion: The present study indicated a novel use of ruscogenin in suppressing HCC metastasis by reducing the expression of MMP-2, MMP-9, uPA, VEGF and HIF-1α via regulating the PI3K/Akt/mTOR signaling pathway.

KEYWORDS

MAPK; blood-brain barrier; inflammasome; ischemic stroke; ruscogenin.

Title

Ruscogenin Suppressed the Hepatocellular Carcinoma Metastasis via PI3K/Akt/mTOR Signaling Pathway

Author

Hui Hua 1 , Yu Zhu 2 , Yu-He Song 3

Publish date

2018 May

PMID

26134424

Abstract

Ruscogenin, a natural steroidal sapogenin, presents in both food and medicinal plants. It has been found to exert significant anti-inflammatory activities. Considering that activation of neutrophil is a key feature of inflammatory diseases, this study was performed to investigate the inhibitory effect of ruscogenin and its underlying mechanisms responsible for neutrophil activation. Ruscogenin displayed potent antioxidative effects against Formyl-Met-Leu-Phe (FMLP)-induced extra- and intracellular superoxide generation in mouse bone marrow neutrophils, with IC50 values of 1.07±0.32 μM and 1.77±0.46 μM, respectively. Phorbol myristate acetate (PMA)-elicited extra- and intracellular superoxide generation were also suppressed by ruscogenin, with IC50 values of 1.56±0.46 μM and 1.29±0.49 μM, respectively. However, ruscogenin showed weak inhibition in NaF-induced response. Inhibition of superoxide generation was mediated neither by a superoxide-scavenging ability nor by a cytotoxic effect. Furthermore, ruscogenin inhibited the membrane translocation of p47phox and p67phox. It reduced FMLP-induced phosphorylation of cytosolic phospholipase A2 (cPLA2) and p21-activated kinase (PAK). The cellular cyclic adenosine monophosphate (cAMP) levels and protein kinase A (PKA) expression were increased by ruscogenin. Moreover, ruscogenin inhibited phosphorylation of protein kinase B (Akt), p38 mitogen-activated protein kinase (p38MAPK), extracellular signal-regulated kinase 1 and 2 (ERK1/2), and c-Jun N-terminal kinase (JNK). In addition, the inhibitory effects of ruscogenin on superoxide production and the phosphorylation of Akt, p38MAPK, and ERK1/2 were reversed by PKA inhibitor (H89), suggesting a PKA-dependent mechanism. In summary, our data suggest that ruscogenin inhibits activation of neutrophil through cPLA2, PAK, Akt, MAPKs, cAMP, and PKA signaling pathways. Increased PKA activity is associated with suppression of the phosphorylation of Akt, p38MAPK, and ERK1/2 pathways.

KEYWORDS

NADPH oxidase; Neutrophils; Ruscogenin; Signaling pathways; Superoxide anion.

Title

Ruscogenin Suppresses Mouse Neutrophil Activation: Involvement of Protein Kinase A Pathway

Author

Y N Lin 1 , R Jia 1 , Y H Liu 1 , Y Gao 1 , L L Wang 1 , J P Kou 2 , B Y Yu 3

Publish date

2015 Nov


Description :

Ruscogenin, an important steroid sapogenin derived from Ophiopogon japonicus, attenuates cerebral ischemia-induced blood-brain barrier dysfunction by suppressing TXNIP/NLRP3 inflammasome activation and the MAPK pathway and exerts significant anti-inflammatory and anti-thrombotic activities[1][2].