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$807

  • Brand : BIOFRON

  • Catalogue Number : BD-P0283

  • Specification : 98.0%(HPLC)

  • CAS number : 36150-23-9

  • Formula : C21H22O6

  • Molecular Weight : 370.4

  • PUBCHEM ID : 182278

  • Volume : 25mg

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Catalogue Number

BD-P0283

Analysis Method

HPLC,NMR,MS

Specification

98.0%(HPLC)

Storage

2-8°C

Molecular Weight

370.4

Appearance

Powder

Botanical Source

Structure Type

Lignans

Category

SMILES

COC1=C(C=C(C=C1)C2C3COC(C3CO2)C4=CC5=C(C=C4)OCO5)OC

Synonyms

5-[(3S,3aR,6S,6aR)-6-(3,4-dimethoxyphenyl)-1,3,3a,4,6,6a-hexahydrofuro[3,4-c]furan-3-yl]-1,3-benzodioxole

IUPAC Name

5-[(3S,3aR,6S,6aR)-6-(3,4-dimethoxyphenyl)-1,3,3a,4,6,6a-hexahydrofuro[3,4-c]furan-3-yl]-1,3-benzodioxole

Applications

Density

Solubility

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

Flash Point

Boiling Point

Melting Point

InChl

InChI=1S/C21H22O6/c1-22-16-5-3-12(7-18(16)23-2)20-14-9-25-21(15(14)10-24-20)13-4-6-17-19(8-13)27-11-26-17/h3-8,14-15,20-21H,9-11H2,1-2H3/t14-,15-,20+,21+/m0/s1

InChl Key

AWOGQCSIVCQXBT-VUEDXXQZSA-N

WGK Germany

RID/ADR

HS Code Reference

2933990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:36150-23-9) 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

27796360

Abstract

Innate immunity has been extended to respond environmental pathogen other than microbial components. Here we explore a novel pollen/TLR4 innate immunity in allergic inflammation. In experimental allergic conjunctivitis induced by short ragweed (SRW) pollen, typical allergic signs, stimulated IL-33/ST2 signaling and overproduced Th2 cytokine were observed in ocular surface, cervical lymph nodes and isolated CD4+ T cells of BALB/c mice. These clinical, cellular and molecular changes were significantly reduced/eliminated in TLR4 deficient (Tlr4-d) or MyD88 knockout (MyD88−/−) mice. Aqueous SRW extract (SRWe) directly stimulated IL-33 mRNA and protein expression by corneal epithelium and conjunctiva in wild type, but not in Tlr4-d or MyD88−/− mice with topical challenge. Furthermore, SRWe-stimulated IL-33 production was blocked by TLR4 antibody and NF-kB inhibitor in mouse and human corneal epithelial cells. These findings for the first time uncovered a novel mechanism by which SRW pollen initiates TLR4-dependent IL-33/ST2 signaling that triggers Th2-dominant allergic inflammation.

Title

Pollen/TLR4 Innate Immunity Signaling Initiates IL-33/ST2/Th2 Pathways in Allergic Inflammation

Author

Jin Li,1,2,* Lili Zhang,2,* Xin Chen,1,2 Ding Chen,1,2 Xia Hua,2 Fang Bian,2 Ruzhi Deng,1 Fan Lu,a,1 Zhijie Li,3 Stephen C. Pflugfelder,2 and De-Quan Lib,2

Publish date

2016;

PMID

29560612

Abstract

Aims
It remains inconclusive whether the use of nonsteroidal anti‐inflammatory drugs (NSAIDs) increases the risk of atrial fibrillation (AF), especially in middle‐aged Asian populations. In this study, we evaluated the association between NSAID use and the risk of AF in a nationwide population‐based study of middle‐aged individuals in Taiwan.

Methods
A nested case-control study was conducted using the National Health Insurance Research Database (NHIRD) in Taiwan. We identified the cases with a diagnosis of AF (ICD‐9‐CM codes: 427.31) and the matched controls from three independent Longitudinal Health Insurance Databases (LHIDs) derived from the NHIRD from data collected from 2001 to 2013. Conditional logistic regression models with covariate adjustment were performed to evaluate the association between NSAID use and the risk of AF.

Results
A total of 57 058 participants (28 529 AF cases and 28 529 matched controls) were included. Participants with NSAID use had an elevated risk of AF compared to non‐users [adjusted odds ratio (AOR) = 1.18, 95% confidence interval (CI): 1.14-1.23]. When further assessing the effects of different classes of NSAIDs on the risk of AF, the results showed that participants who used non‐selective NSAIDs had a significantly elevated risk of AF (AOR = 1.18, 95% CI: 1.13-1.23), as did participants with a combined use of selective and non‐selective NSAIDs (AOR = 1.30, 95% CI: 1.21-1.39).

Conclusions
NSAID use was associated with an increased risk of AF occurrence among the participants included in our study cohort. Closely monitoring the adverse effects of NSAID treatment on the risk of AF will be important, particularly among individuals at high risk.

KEYWORDS

atrial fibrillation, middle‐aged population, nationwide population‐based study, nonsteroidal anti‐inflammatory drugs

Title

Association between nonsteroidal anti‐inflammatory drugs and atrial fibrillation among a middle‐aged population: a nationwide population‐based cohort

Author

Shao‐Yuan Chuang, 1 Pai‐Feng Hsu, 2 , 3 , 4 Fang‐Ju Lin, 5 , 6 , 7 Ya‐Wen Huang, 1 Gou‐Zhau Wang, 8 Wei‐Chiao Chang, 9 , 10 , 11 , 12 and Hui‐Ju Tsaicorresponding author 1 , 13

Publish date

2018 Jun

PMID

25384983

Abstract

Hemichannels (HCs) are hexamers of connexins that can form gap-junction channels at points of cell contacts or “free HCs” at non-contacting regions. HCs are involved in paracrine and autocrine cell signaling, and under pathological conditions may induce and/or accelerate cell death. Therefore, studies of HC regulation are of great significance. Nitric oxide affects the activity of Cx43 and Cx46 HCs, whereas carbon monoxide (CO), another gaseous transmitter, modulates the activity of several ion channels, but its effect on HCs has not been explored. We studied the effect of CO donors (CORMs) on Cx46 HCs expressed in Xenopus laevis oocytes using two-electrode voltage clamp and on Cx43 and Cx46 expressed in HeLa cells using a dye-uptake technique. CORM-2 inhibited Cx46 HC currents in a concentration-dependent manner. The C-terminal domain and intracellular Cys were not necessary for the inhibition. The effect of CORM-2 was not prevented by guanylyl-cyclase, protein kinase G, or thioredoxin inhibitors, and was not due to endocytosis of HCs. However, the effect of CORM-2 was reversed by reducing agents that act extracellularly. Additionally, CO inhibited dye uptake of HeLa cells expressing Cx43 or Cx46, and MCF-7 cells, which endogenously express Cx43 and Cx46. Because CORM-2 carbonylates Cx46 in vitro and induces conformational changes, a direct effect of that CO on Cx46 is possible. The inhibition of HCs could help to understand some of the biological actions of CO in physiological and pathological conditions.

KEYWORDS

Carbon Monoxide, Connexin, Ion Channel, Post-translational Modification (PTM), Redox Signaling, Carbonylation, Hemichannels

Title

Carbon Monoxide (CO) Is a Novel Inhibitor of Connexin Hemichannels*

Author

Carmen G. Leon-Paravic,‡ Vania A. Figueroa,‡ Diego J. Guzman,‡ Carlos F. Valderrama,‡ Antonio A. Vallejos,‡ Mariana C. Fiori,§ Guillermo A. Altenberg,§ Luis Reuss,§ and Mauricio A. Retamal‡§,1

Publish date

2014 Dec 26;