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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


Description :

Plantamajoside Inhibits UVB and Advanced Glycation End Products-Induced MMP-1 Expression by Suppressing the MAPK and NF-κB Pathways in HaCaT Cells. PUMID/DOI:27346084 Photochem Photobiol. 2016 Sep;92(5):708-19. Photoaging and glycation stress are major causes of skin deterioration. Oxidative stress caused by ultraviolet B (UVB) irradiation can upregulate matrix metalloprotease 1 (MMP-1), a major enzyme responsible for collagen damage in the skin. Advanced glycation end products (AGEs) accumulate via gradual formation from skin proteins, especially from long-lived proteins such as dermal elastin and collagen. Plantamajoside (PM), isolated from Plantago asiatica, has various biological effects including anti-inflammatory and antioxidant effects. In this study, we assessed the protective effects of PM on a human keratinocyte cell line (HaCaT) and primary human dermal fibroblasts (HDF) against stress caused by glyceraldehyde-induced AGEs (glycer-AGEs) with UVB irradiation. We found that PM attenuated UVB- and-glycer-AGEs-induced MMP-1 expression in HaCaT and HDF cells and proinflammatory cytokines expression by inhibiting the phosphorylation of mitogen-activated protein kinases (MAPKs) activated by reactive oxygen species. Specific inhibitors of NF-κB and MAPKs attenuated the induced expression of MMP-1. PM also inhibited the phosphorylation of IκBα, and reduced nuclear translocation of NF-κB in these cells. Furthermore, PM attenuated the upregulation of receptor for AGEs (RAGE) by glycer-AGEs with UVB irradiation. Therefore, our findings strongly suggest that PM is a promising inhibitor of skin photoaging. Nephroprotection of plantamajoside in rats treated with cadmium. PUMID/DOI:25499790 Environ Toxicol Pharmacol. 2015 Jan;39(1):125-36. Plantamajoside (PMS), a major compound of Plantago asiatica (PA), was reported to have the antioxidant effects. In this study, we investigated the protective effects of PMS on Cadmium-induced renal damage in the NRK-52E cell and rat kidney tissue. Cadmium exposure increased the ROS generation, lipid peroxidation, serum biochemical values of renal damage, and mRNA and protein expressions of KIM-1 in vitro and in vivo. The significant reduction in glutathione (GSH)/glutathione disulfide (GSSG) ratio and activities of antioxidant enzymes were also observed in the rats treated with Cadmium. Plantamajoside significantly decreased the ROS generation and lipid peroxidation, thus enhancing GSH/GSSG ratio, antioxidant enzyme activities in the cells and rats, and improved histochemical appearances, indicating that Plantamajoside has protective activities against Cadmium-induced renal injury. Plantamajoside ameliorates lipopolysaccharide-induced acute lung injury via suppressing NF-κB and MAPK activation. PUMID/DOI:27089391 Int Immunopharmacol. 2016 Jun;35:315-322. 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. A 90 day repeated oral toxicity study on plantamajoside concentrate from Plantago asiatica. PUMID/DOI:17622978 Phytother Res. 2007 Dec;21(12):1118-23. Plantago asiatica is distributed widely in East Asia. Since ancient times it has been used as a diuretic to treat acute urinary infections, and as an antiinflammatory, antiasthmatic, antioxidant, antibacterial, antihyperlipidemic and antihepatitis drug. The major compound, Plantamajoside from P. asiatica, which is used as a marker compound in chemotaxonomic studies, was reported to have antibacterial activity, inhibition activity against cAMP phosphodiesterase and 5-lipoxygenase and antioxidant activity. Plantamajoside, a potential anti-tumor herbal medicine inhibits breast cancer growth and pulmonary metastasis by decreasing the activity of matrix metalloproteinase-9 and -2. PUMID/DOI:26674531 BMC Cancer. 2015 Dec 16;15:965. Metastasis is the major cause of death in breast cancers. MMPs play a key role in tumor microenvironment that facilitates metastasis. The existing researches suggest that the high expression of gelatinase A and B (MMP2 and MMP9) promote the metastasis of breast cancer. Therefore, gelatinase inhibitor can effectively suppress tumor metastasis. However, at present, there is no dramatically effective gelatinase inhibitor against breast cancer.We successfully screened an Chinese herbal medicine-Plantamajoside(PMS)-which can reduce the gelatinase activity of MMP9 and MMP2. In vitro, PMS can inhibit the proliferation, migration and invasion of MDA-MB-231 human breast cancer cell line and 4T1 mouse breast cancer cell line by decreasing MMP9 and MMP2 activity. In vivo, oral administration of PMS to the mice bearing 4T1 cells induced tumors resulted in significant reduction in allograft tumor volume and weights, significant decrease in microvascular density and significant lower lung metastasis rate.||CONCLUSIONS:||Our results indicate that as a promising anti-cancer agent, PMS may inhibit growth and metastasis of breast cancer by inhibiting the activity of MMP9 and MMP2.