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2-Methoxycinnamaldehyde

$120

  • Brand : BIOFRON

  • Catalogue Number : BN-O1387

  • Specification : 98%(HPLC)

  • CAS number : 1504-74-1

  • Formula : C10H10O2

  • Molecular Weight : 162.19

  • PUBCHEM ID : 641298

  • Volume : 20mg

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Catalogue Number

BN-O1387

Analysis Method

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

162.19

Appearance

Powder

Botanical Source

This product is isolated and purified from the barks of Cinnamomum cassia Presl

Structure Type

Category

SMILES

COC1=CC=CC=C1C=CC=O

Synonyms

3-(2-Methoxyphenyl)acrylaldehyde/2-Methoxycinnamaldehyde/(2E)-3-(2-Methoxyphenyl)acrylaldehyde/2-Propenal, 3- (2-methoxyphenyl)-/β-(o-Methoxyphenyl)acrolein/o-Methoxycinnamaldehyde/o-Methoxycinnamicaldehyde crystals/(2E)-3-(2-Methoxyphenyl)Prop-2-Enal/2-Propenal, 3-(2-methoxyphenyl)-, (2E)-

IUPAC Name

Density

1.1±0.1 g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

134.4±13.9 °C

Boiling Point

334.8±0.0 °C at 760 mmHg

Melting Point

44-48ºC

InChl

InChl Key

KKVZAVRSVHUSPL-GQCTYLIASA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:1504-74-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

27922672

Abstract

The abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) is a crucial event in the development of atherosclerosis, and tumor necrosis factor-α (TNF-α) is actively involved in this process by enhancing the proliferation and migration of VSMCs. 2-Methoxycinnamaldehyde (MCA) is a natural compound of Cinnamomum cassia. Although 2-hydroxycinnamaldehyde (HCA), another compound from Cinnamomum cassia, has been widely studied with regard to its antitumor activity, MCA has not attracted researchers’ interest due to its mild toxic effects on cancer cells and its mechanisms of action remain unknown. In this study, we examined the effects of MCA on the TNF-α-induced proliferation and migration of human aortic smooth muscle cells (HASMCs). As shown by our results, MCA inhibited TNF-α-induced cell proliferation by reducing the levels of cyclin D1, cyclin D3, CDK4 and CDK6, and increasing the levels of the cyclin-dependent kinase inhibitors, p21 and p27, without resulting in cellular cytotoxicity. Furthermore, MCA decreased the level of secreted matrix metalloproteinase (MMP)-9 by inhibiting MMP-9 transcription. Unexpectedly, MCA did not affect the TNF-α-induced levels of mitogen-activated protein kinases (MAPKs). However, by showing that MCA potently inhibited the degradation of IκBα and the subsequent nuclear translocation of nuclear factor-κB (NF-κB), we demonstrated that MCA exerts its effects through the NF-κB signaling pathway. MCA also effectively inhibited platelet-derived growth factor (PDGF)-induced HASMC migration. Taken together, these observations suggest that MCA has the potential for use as an anti-atherosclerotic agent.

Title

2-Methoxycinnamaldehyde inhibits the TNF-α-induced proliferation and migration of human aortic smooth muscle cells.

Author

Jin YH1, Kim SA1.

Publish date

2017 Jan

PMID

32133057

Abstract

OBJECTIVES:
Hepatic ischemia/reperfusion injury (IRI) is one of the major causes of hepatic failure during liver transplantation, trauma, and infections. The present study investigated the protective effect of intra-portal administration of 2-methoxycinnamaldehyde (2-MCA) on hepatic IRI in rats.

MATERIALS AND METHODS:
Twenty-four rats were equally divided into four groups; 1) sham group, (no IRI or transfusion), 2) Hepatic IRI (60 min ischemia + 120 min reperfusion, 3) Hepatic IRI+ NS (IRI + normal saline), 4) Hepatic IRI+2-MCA, (IRI + 2-MCA). In groups 3 and 4, 1 ml/kg normal saline and 2-MCA were administered slowly into the vein of the left lateral and median lobes of the liver 10 min before induction of hepatic reperfusion (upper the site of clumping), respectively. The harvest time points were at 2 hours post-reperfusion in all groups.

RESULTS:
Histologically, cell death, degenerative changes, sinusoidal dilatation, congestion, hemorrhage, and infiltration of inflammatory cells were observed in IRI group, while these pathological changes were attenuated in the 2-MCA administrated group. The level of alanine transaminase, aspartate transaminase, tumor necrosis factor- α and interleukin-6 in serum and hepatic malondialdehyde were significantly increased by IRI, and 2-MCA administration reduced all these markers. In addition, caspase-3 and nuclear factor κB (NF-κB) expression were investigated immunohistochemically. Administration of 2-MCA considerably decreased caspase-3 positive cells and NF-κB activity in comparison with IRI group.

CONCLUSION:
As a conclusion, in situ administration of 2-MCA protects against hepatic IRI via anti-inflammatory, and anti-apoptotic properties.

KEYWORDS

Ischemia reperfusion injury; Liver; Oxidative stress; Rat 2-Methoxycinnamaldehyde

Title

Protective effects of 2-methoxycinnamaldehyde an active ingredients of Cinnamomum cassia on warm hepatic ischemia reperfusion injury in rat model.

Author

Golshahi H1, Araghi A2, Baghban F3, Farzad-Mohajeri S4,5.

Publish date

2019 Dec

PMID

22179023

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE:
Cinnamomum cassia Blume has been used as a traditional Chinese herbal medicine for alleviation of fever, inflammation, chronic bronchitis, and to improve blood circulation.

AIM OF THE STUDY:
We addressed whether 2-methoxycinnamaldehyde (2-MCA), one of active ingredients of Cinnamomum cassia, reduces vascular cell adhesion molecule-1 (VCAM-1) expression in tumor necrosis factor-alpha (TNF-α)-activated endothelial cells and protects ischemia/reperfusion (I/R)-injury due to heme oxygenase (HO)-1 induction.

MATERIALS AND METHODS:
Adult male rats were subjected to 30 min of ischemia by occlusion of the left anterior descending coronary artery followed by 24h of reperfusion. Rats were randomized to receive vehicle or 2-MCA (i.v.) 10 min before reperfusion.

RESULTS:
Administration of 2-MCA significantly improved I/R-induced myocardial dysfunction by increasing the values of the first derivative (±dp/dt) of left ventricular pressure and decreased infarct size. In addition, 2-MCA reduced the expression of high mobility group box 1 (HMGB1), an activator of the inflammatory cascade when released into the extracellular space, and VCAM-1 in I/R myocardium along with increase of HO-1 induction. The reduced injury was accompanied by significantly reduction of neutrophils infiltration and increased SOD activity in ischemic tissues and reduced serum level of cardiac troponin I (cTnI). Furthermore, 2-MCA significantly increased HO-1 induction by translocation of Nrf-2 from cytosol to nucleus in endothelial cells. Inhibition of VCAM-1 expression by 2-MCA was reversed both by SnPPIX, a HO-1 inhibitor and siHO-1 RNA trasfection in TNF-α-activated cells. In addition, 2-MCA significantly inhibited NF-κB luciferase activity in TNF-α-activated endothelial cells. As expected, 2-MCA significantly inhibited monocyte (U937) adhesion to endothelial cells.

CONCLUSION:
We concluded that 2-MCA protects of myocardial I/R-injury due to antioxidant and anti-inflammatory action possibly by HO-1 induction which can be explained why Cinnamomum cassia has been used in inflammatory disorders.

Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

Title

2-methoxycinnamaldehyde from Cinnamomum cassia reduces rat myocardial ischemia and reperfusion injury in vivo due to HO-1 induction.

Author

Hwa JS1, Jin YC, Lee YS, Ko YS, Kim YM, Shi LY, Kim HJ, Lee JH, Ngoc TM, Bae KH, Kim YS, Chang KC.

Publish date

2012 Jan 31


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