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Morin

$87

  • Brand : BIOFRON

  • Catalogue Number : BD-D0930

  • Specification : HPLC≥98%

  • CAS number : 654055-01-3

  • Formula : C15H12O8

  • Molecular Weight : 320.25

  • PUBCHEM ID : 16219651

  • Volume : 20mg

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Catalogue Number

BD-D0930

Analysis Method

Specification

HPLC≥98%

Storage

2-8°C

Molecular Weight

320.25

Appearance

Botanical Source

Structure Type

Category

SMILES

C1=CC(=C(C=C1O)O)C2=C(C(=O)C3=C(C=C(C=C3O2)O)O)O.O

Synonyms

2-(2,4-Dihydroxyphenyl)-3,5,7-trihydroxy-4H-chromen-4-one hydrate (1:1)/S2325_Selleck/Morin hydrate/2',3,4',5,7-pentahydroxyflavone/4H-1-Benzopyran-4-one, 2-(2,4-dihydroxyphenyl)-3,5,7-trihydroxy-, hydrate (1:1)/2-(2,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-1-benzopyran-4-one/Bois d,arc hydrate

IUPAC Name

2-(2,4-dihydroxyphenyl)-3,5,7-trihydroxychromen-4-one;hydrate

Density

Solubility

Flash Point

Boiling Point

Melting Point

299-300 °C (dec.)(lit.)

InChl

InChl Key

MYUBTSPIIFYCIU-UHFFFAOYSA-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#:654055-01-3) 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

29197568

Abstract

We report here the inhibition of amyloid fibrillation of human insulin in vitro by Morin hydrate, a naturally occurring small molecule. Using spectroscopic assays and transmission electron microscopy, we found that Morin hydrate effectively inhibits insulin amyloid fibrillation in a dose dependent manner with more than 80% inhibition occurring even at only a 1:1 concentration. As suggested by fluorescence spectroscopic titration studies, Morin hydrate binds to insulin with a fairly strong affinity of -26.436kJmol-1. Circular dichroism (CD) spectroscopy was used to analyse structural changes of insulin in the presence of Morin hydrate demonstrating the ability of Morin hydrate to bind with the native monomeric protein and/or its near native state, intermediate oligomeric species and amyloid fibrils. Based on computational docking and molecular dynamics study, we propose that Morin hydrate binds to residues having greater aggregation propensity and prevent structural and/or conformational changes leading to amyloid fibrillation. Morin hydrate should also bind to fibrils by hydrogen bonding and/or hydrophobic forces throughout the surface, stabilize them and inhibit the release of oligomeric species which could be nuclei or template for further fibrillation. Overall results provide an insight into the mechanism of inhibition of insulin amyloid fibrillation by Morin hydrate.

Copyright © 2017 Elsevier B.V. All rights reserved.

KEYWORDS

Aggregation propensity; Computational docking; Insulin amyloid fibrillation; Molecular dynamics; Morin hydrate

Title

Inhibition of insulin amyloid fibrillation by Morin hydrate.

Author

Patel P1, Parmar K2, Das M3.

Publish date

2018 Mar

PMID

31311167

Abstract

Chemoresistance is a major obstacle that limits the benefits of cisplatin-based chemotherapy in various cancers, including hepatocellular carcinoma. De-regulation of the poly(ADP-ribose) polymerase 1 (PARP1)/high-mobility group box 1 (HMGB1) signaling pathway has been proposed as an important mechanism involved in cisplatin-resistance. In this study, we investigated therapeutic potential of a natural flavonoid Morin hydrate against cisplatin-induced toxicity using the HepG2DR multi-drug resistant cell line, which is derived from the HepG2 human hepatocellular carcinoma cell line. HepG2DR cells were exposed to cisplatin and Morin hydrate alone or together after which autophagy and apoptotic signaling pathways were monitored by fluorometric assay and Western blot analysis. Xenograft mouse models were performed to confirm the in vitro effect of Morin hydrate. PARP1 was hyper activated in cisplatin-resistant HepG2DR cells. Cisplatin-induced PARP1 activation resulted in chemoresistance via increased autophagy. The cisplatin/Morin hydrate combination was effective in the reversal of the HepG2DR cell resistance via suppression of PARP1-mediated autophagy by regulating the HMGB1 and microtubule-associated protein 1A/1B light chain 3B (LC3) I/II. Moreover, PARP1 inhibition by 4-amino-1,8-naphthalimide or autophagy inhibition by a knockdown of the autophagy-related 5 (Atg5) gene resulted in sensitizing the HepG2DR cells to cisplatin (CP) through activation of the c-Jun N-terminal kinase (JNK) pathway. In a mouse xenograft model, the treatment of cisplatin with Morin hydrate reversed the increased expression of PARP and HMGB1 and significantly suppressed tumor growth. These findings indicate dysregulated expression of PARP1 confers cisplatin-resistance via autophagy activation in HepG2DR cells. Morin hydrate inhibits cisplatin-mediated autophagy induction, resulting in increased susceptibility of HepG2DR cells to cisplatin cytotoxicity. The combination of Morin hydrate with cisplatin may be a promising therapeutic strategy to enhance the efficacy of conventional chemotherapeutic drugs.

KEYWORDS

Morin hydrate; PARP1; autophagy; chemoresistance; cisplatin; hepatocellular carcinoma

Title

Morin Hydrate Reverses Cisplatin Resistance by Impairing PARP1/HMGB1-Dependent Autophagy in Hepatocellular Carcinoma.

Author

Singh MP1, Cho HJ2, Kim JT2, Baek KE2, Lee HG3,4, Kang SC5.

Publish date

2019 Jul 15

PMID

30034650

Abstract

INTRODUCTION:
As stress affects the brain both physiologically and chemically, researchers try to find novel anti-stress compounds with beneficial therapeutic effects. In this regard, the effect of stress and its modulation by Morin hydrate was studied using different acute models in mice.

METHODS:
The models employed were anoxic tolerance, swimming endurance, and acute restraint test. Morin hydrate or the vehicle was administered 30 minutes prior to each stress exposure while in the acute restraint test; the animals were pretreated for 7 days with Morin hydrate, vehicle, imipramine, or diazepam before stress exposure. The measured parameters were the onset of convulsion and immobility time in the anoxic tolerance and swimming endurance test, respectively, while in the acute restraint test, the animals were assessed for stress-induced anxiety using the elevated plus maze and depression using the forced swim test. Thereafter blood was withdrawn from the retro-orbital plexus and plasma separated, the brain was also isolated, homogenized, centrifuged, and the supernatant was obtained for biochemical estimation.

RESULTS:
Morin hydrate (5, 10, 20 mg/kg) produced a significant reduction in immobility time in the swimming endurance test, while significantly increased the anoxic stress tolerance time. Acute restraint stress caused a significant decrease in reduced glutathione levels (which was reversed by Morin hydrate) and increased the level of malondialdehyde, a thiobarbituric acid reactive substance which is an index of oxidative stress and nitrite. These effects were attenuated by Morin hydrate. Also, pretreatment with Morin hydrate attenuates acute restraint stress-associated anxiety and depression, reversed the hyperglycemia evoked by the stressful exposure and normalized serum cholesterol levels.

CONCLUSION:
These findings suggest that Morin hydrate exhibits anti-stress effects and may be useful in the relief of stress.

KEYWORDS

Anxiety; Depression; Morin hydrate; Restraint; Stress

Title

Protective Effects of Morin Hydrate on Acute Stress-Induced Behavioral and Biochemical Alterations in Mice.

Author

Olonode ET1,2, Aderibigbe AO2, Adeoluwa OA1, Ajayi AM2.

Publish date

2018 May-Jun


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