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Plantamajoside

$113

Brand : BIOFRON
Catalogue Number : BF-P2018
Specification : 98%
CAS number : 104777-68-6
Formula : C29H36O16
Molecular Weight : 640.59
PUBCHEM ID : 5281788
Volume : 20mg

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Catalogue Number

BF-P2018

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

640.59

Appearance

White crystalline powder

Botanical Source

Plantago asiatica,Lagotis brevituba,Plantago depressa

Structure Type

Phenylpropanoids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC(=C(C=C1CCOC2C(C(C(C(O2)CO)OC(=O)C=CC3=CC(=C(C=C3)O)O)OC4C(C(C(C(O4)CO)O)O)O)O)O)O

Synonyms

purpureaside A/β-D-Glucopyranoside, 2-(3,4-dihydroxyphenyl)ethyl 4-O-[(2E)-3-(3,4-dihydroxyphenyl)-1-oxo-2-propen-1-yl]-3-O-β-D-glucopyranosyl-/Y0160/Plantamajoside/2-(3,4-Dihydroxyphenyl)ethyl 4-O-[(2E)-3-(3,4-dihydroxyphenyl)-2-propenoyl]-3-O-β-D-glucopyranosyl-β-D-glucopyranoside

IUPAC Name

[(2R,3R,4R,5R,6R)-6-[2-(3,4-dihydroxyphenyl)ethoxy]-5-hydroxy-2-(hydroxymethyl)-4-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyoxan-3-yl] (E)-3-(3,4-dihydroxyphenyl)prop-2-enoate

Density

1.7±0.1 g/cm3

Solubility

Methanol; Water; Acetontrile

Flash Point

308.5±27.8 °C

Boiling Point

953.0±65.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C29H36O16/c30-11-19-22(37)23(38)24(39)29(42-19)45-27-25(40)28(41-8-7-14-2-5-16(33)18(35)10-14)43-20(12-31)26(27)44-21(36)6-3-13-1-4-15(32)17(34)9-13/h1-6,9-10,19-20,22-35,37-40H,7-8,11-12H2/b6-3+/t19-,20-,22-,23+,24-,25-,26-,27-,28-,29+/m1/s1

InChl Key

KFEFLPDKISUVNR-QJEHNBJNSA-N

WGK Germany

RID/ADR

HS Code Reference

2938900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:104777-68-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

29710521

Abstract

Plantamajoside (PMS) is a major compound of Plantago asiatica and possesses anti-tumor activity. However, the effect of PMS on esophageal squamous cell carcinoma (ESCC) and the underlying mechanism of action are unclear. The present study aimed to evaluate the effect of PMS on lipopolysaccharide (LPS)-induced epithelial-mesenchymal transition (EMT) in ESCC. The results showed that PMS inhibited viability of ESCC cell lines (Eca-109 and TE-1) in a concentration-dependent manner. PMS also inhibited LPS-induced EMT in ESCC cells. PMS inhibited LPS-induced activation of the NF-κB pathway and IL-6 expression. PMS also suppressed IL-6-induced EMT in ESCC cells. Treatment of BAY11-7082 (an inhibitor of NF-κB) or antibody against IL-6 alleviated the effect of LPS-induced EMT in ESCC cells. Besides, inhibition of NF-κB decreased IL-6 expression. In conclusion, the results indicated that PMS inhibited LPS-induced EMT through suppressing the NF-κB/IL-6 signaling in ESCC cell lines, suggesting that PMS might be a useful agent for the treatment of ESCC.

KEYWORDS

Epithelial-mesenchymal transition; Esophageal squamous cell carcinoma; IL-6; NF-κB; Plantamajoside.

Title

Plantamajoside Inhibits Lipopolysaccharide-Induced Epithelial-Mesenchymal Transition Through Suppressing the NF-κB/IL-6 Signaling in Esophageal Squamous Cell Carcinoma Cells

Author

Xiaohui Li 1 , Dong Chen 1 , Mengfei Li 1 , Xiang Gao 1 , Gongning Shi 1 , Hui Zhao 2

Publish date

2018 Jun

PMID

30476578

Abstract

Periodontitis is an important inflammatory disease that often causes by periodontopathic bacteria. The present study, we tested the anti-inflammatory effects of plantamajoside on LPS-stimulated human gingival fibroblasts. Human gingival fibroblasts (HGFs) were stimulated with LPS from Porphyromonas gingivalis. Plantamajoside was administrated 1 h before LPS treatment. The results demonstrated that plantamajoside decreased the production of PGE2, NO, IL-6, and IL-8 in LPS-stimulated HGFs. LPS-induced NF-κB p65 and IκB phosphorylation were also suppressed by plantamajoside. Furthermore, plantamajoside inhibited LPS-induced PI3K and AKT phosphorylation. In conclusion, these results suggested that the mechanism of plantamajoside was through inhibiting PI3K/AKT signaling pathway, which lead to the inhibition of NF-κB activation and inflammatory response.

KEYWORDS

Human gingival fibroblasts; IL-8; LPS; PI3K; Plantamajoside.

Title

Plantamajoside Attenuates Inflammatory Response in LPS-stimulated Human Gingival Fibroblasts by Inhibiting PI3K/AKT Signaling Pathway

Author

Fei Liu 1 , Xin Huang 2 , Jing-Jun He 3 , Ci Song 4 , Ling Peng 4 , Ting Chen 5 , Bu-Ling Wu 6

Publish date

2019 Feb

PMID

27089391

Abstract

Despite developments in the knowledge and therapy of acute lung injury in recent decades, mortality remains high, and there is usually a lack of effective therapy. Plantamajoside, a major ingredient isolated from Plantago asiatica L. (Plantaginaceae), has been reported to have potent anti-inflammatory properties. However, the effect of plantamajoside on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice has not been investigated. The present study aimed to reveal the potential mechanism responsible for the anti-inflammatory effects of plantamajoside on LPS-induced acute lung injury in mice and in RAW264.7 cells. The results of histopathological changes as well as the lung wet-to-dry ratio and myeloperoxidase (MPO) activity showed that plantamajoside ameliorated the lung injury that was induced by LPS. qPCR and ELISA assays demonstrated that plantamajoside suppressed the production of IL-1β, IL-6 and TNF-α in a dose-dependent manner. TLR4 is an important sensor in LPS infection. Molecular studies showed that the expression of TLR4 was inhibited by plantamajoside administration. Further study was conducted on nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) using pathways using western blots. The results showed that plantamajoside inhibited the phosphorylation of IκBα, p65, p38, JNK and ERK. All results indicated that plantamajoside has protective effect on LPS-induced ALI in mice and in RAW264.7 cells. Thus, plantamajoside may be a potential therapy for the treatment of pulmonary inflammation.

KEYWORDS

Acute lung injury; Anti-inflammation; MAPK; NF-κB; Plantamajoside.

Title

Plantamajoside Ameliorates Lipopolysaccharide-Induced Acute Lung Injury via Suppressing NF-κB and MAPK Activation

Author

Haichong Wu 1 , Gan Zhao 1 , Kangfeng Jiang 1 , Xiuying Chen 1 , Zhe Zhu 1 , Changwei Qiu 1 , Chengye Li 1 , Ganzhen Deng 2

Publish date

2016 Jun