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Corynoxine

$640

Brand : BIOFRON
Catalogue Number : BD-D0958
Specification : HPLC≥98%
CAS number : 6877-32-3
Formula : C22H28N2O4
Molecular Weight : 384.46
PUBCHEM ID : 10475115
Volume : 20mg

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Catalogue Number

BD-D0958

Analysis Method

HPLC,NMR,MS

Specification

HPLC≥98%

Storage

2-8°C

Molecular Weight

384.46

Appearance

White crystalline powder

Botanical Source

Uncaria rhynchophylla(Miq.)Miq. ex Havil./Alkaloid from Pseudocinchona africana, Uncaria macrophylla and Mitragyna speciosa (Rubiaceae, Naucleaceae)

Structure Type

Indoles

Category

Standards;Natural Pytochemical;API

SMILES

CCC1CN2CCC3(C2CC1C(=COC)C(=O)OC)C4=CC=CC=C4NC3=O

Synonyms

Methyl (16E)-16-(methoxymethylene)-2-oxocorynoxan-17-oate/Spiro[3H-indole-3,1'(5'H)-indolizine]-7'-acetic acid, 6'-ethyl-1,2,2',3',6',7',8',8'a-octahydro-α-(methoxymethylene)-2-oxo-, methyl ester, (αE,3S,6'S,7'S,8'aS)-

IUPAC Name

methyl (E)-2-[(3S,6'S,7'S,8'aS)-6'-ethyl-2-oxospiro[1H-indole-3,1'-3,5,6,7,8,8a-hexahydro-2H-indolizine]-7'-yl]-3-methoxyprop-2-enoate

Density

1.2±0.1 g/cm3

Solubility

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

Flash Point

293.0±30.1 °C

Boiling Point

560.8±50.0 °C at 760 mmHg

Melting Point

166-168ºC

InChl

InChI=1S/C22H28N2O4/c1-4-14-12-24-10-9-22(17-7-5-6-8-18(17)23-21(22)26)19(24)11-15(14)16(13-27-2)20(25)28-3/h5-8,13-15,19H,4,9-12H2,1-3H3,(H,23,26)/b16-13+/t14-,15+,19+,22+/m1/s1

InChl Key

DAXYUDFNWXHGBE-NRAMRBJXSA-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#:6877-32-3) 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

31610203

Abstract

BACKGROUND:
The protective effects of gastrodin and rhynchophylline in ischaemic injury have been reported. However, the underlying mechanism and the effect of the combination of these two drugs in ischaemic injury remain unclear. Herein, we aimed to explore the effects of the combination of gastrodin and rhynchophylline on ischaemia-induced inflammasome activation as well as the underlying mechanism.

METHODS:
Middle cerebral artery occlusion (MCAO) mice and oxygen glucose deprivation (OGD)-treated BV2 cells were used as in vivo and in vitro models of ischaemia, respectively. Cerebral injury was determined by TTC staining, H&E staining and neurological deficit scores. The effects of the combination of gastrodin and rhynchophylline on inflammasome activation were measured by the MTT assay, Western blotting and ELISA. The expression of miR-21-5p and miR-331-5p was measured by qRT-PCR. The potential binding between miR-21-5p and TXNIP and between miR-331-5p and TRAF6 was analysed with Targetscan and a luciferase assay.

RESULTS:
MCAO-induced tissue infarction, neurological deficits, inflammasome activation, and downregulation of miR-21-5p and miR-331-5p were all mitigated by the combination of gastrodin and rhynchophylline. In OGD-treated BV2 cells, the combination of gastrodin and rhynchophylline also alleviated inflammasome activation and restored the expression of miR-21-5p and miR-331-5p. TXNIP and TRAF6 were confirmed to be targets of miR-21-5p and miR-331-5p, respectively. Moreover, OGD-induced inflammasome activation was attenuated by the overexpression of either miR-331-5p or miR-21-5p and was further attenuated by the overexpression of both. Finally, we demonstrated that a miR-21-5p inhibitor and/or a miR-331-5p inhibitor counteracted the protective effects of gastrodin and/or rhynchophylline.

CONCLUSIONS:
The combination of gastrodin and rhynchophylline exerts neuroprotective effects by preventing ischaemia-induced inflammasome activation via upregulating miR-21-5p and miR-331-5p.

Copyright © 2019 Elsevier Inc. All rights reserved.

KEYWORDS

Gastrodin; Inflammasome; Rhynchophylline; miR-21-5p; miR-331-5p

Title

Gastrodin combined with rhynchophylline inhibits cerebral ischaemia-induced inflammasome activation via upregulating miR-21-5p and miR-331-5p

Author

Zhang HS1, Liu MF1, Ji XY2, Jiang CR3, Li ZL3, OuYang B4.

Publish date

2019 Dec

PMID

31420791

Abstract

Migraine causes severe health and social issues worldwide. Rhynchophylline (Rhy) is one of the major active components of Uncaria rhynchophylla that is used for the treatment of headache in Traditional Chinese Medicine. In the current study, the effect of Rhy on nitroglycerin (NTG)-induced migraine was assessed and the associated mechanism was also explored to explain its function. Rats were pre-treated with Rhy of two doses (10 mg/kg and 30 mg/kg) and then subjected to NTG to induce migraine symptoms. Thereafter, the electroencephalogram (EEG) signaling, spontaneous behaviors, levels of indicators related to oxidative stress, and expression of calcitonin gene-related peptide (CGRP) were measured to assess the anti-migraine function of Rhy. Moreover, the activities of MAPK/NF-κB pathway under the administrations of Rhy were also detected. The results showed that NTG induced EEG and behavior disorders in rats, which was associated with the initiation of oxidative stress and increased expression of CGRP. Nevertheless, the pre-treatments with Rhy attenuated the damages induced by NTG by reversing the levels of all the above indicators. The results of western blotting demonstrated that the anti-migraine effect of Rhy was accompanied by the inhibition of MAPK/NF-кB pathway. The findings outlined in the current study revealed an alternative mechanism of Rhy in protecting brain tissues against migraine: the agent exerted its effect by suppressing MAPK/NF-кB pathway, which would ameliorate impairments associated with migraine.

KEYWORDS

Migraine; NF-кB; Nitroglycerin; Oxidative stress; Rhynchophylline

Title

Rhynchophylline attenuates migraine in trigeminal nucleus caudalis in nitroglycerin-induced rat model by inhibiting MAPK/NF-кB signaling.

Author

Lai T1, Chen L1, Chen X1, He J2, Lv P3, Ge H4.

Publish date

2019 Nov

PMID

31231976

Abstract

The aim of this study was designed to investigate the effects of rhynchophyllin (RH) on neuroinflammation in Tourette syndrome (TS) rats. TS model was established in rats by the injection of selective 5-HT2A/2C agonist 1-(2, 5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI). Behavior in DOI-induced rats was tested. Inflammatory cytokines levels such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in serum and striatum were detected. The expression levels of janus kinase 2 (JAK2)/signal transducer and transcription activator 3 (STAT3) and nuclear factor (NF)-κB pathways in striatum were measured by Western blot. Data indicated that RH can significantly reduce the numbers of nodding experiment of TS rats. RH significantly decreased IL-6, IL-1β, and TNF-α in serum and striatum of TS rats, with altered expression of P-JAK2, P-STAT3, P-NF-κBp65, and P-IκBα in TS rats, as evidenced by Western blot analysis and immunohistochemistry, suggesting that the regulation of JAK2/STAT3 and NF-κB pathways might be involved in the mechanism of RH on TS.

© 2019 Wiley Periodicals, Inc.

KEYWORDS

JAK2/STAT3; NF-κB; Tourette syndrome; neuroinflammation; rhynchophyllin

Title

Rhynchophyllin attenuates neuroinflammation in Tourette syndrome rats via JAK2/STAT3 and NF-κB pathways.

Author

Hongyan L1, Mengjiao Z2, Chunyan W2, Yaruo H2.

Publish date

2019 Oct;