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Dihydrotanshinone I

$225

  • Brand : BIOFRON

  • Catalogue Number : BF-D3005

  • Specification : 95%

  • CAS number : 87205-99-0

  • Formula : C18H14O3

  • Molecular Weight : 278.3

  • PUBCHEM ID : 11425923

  • Volume : 100mg

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Catalogue Number

BF-D3005

Analysis Method

HPLC,NMR,MS

Specification

95%

Storage

2-8°C

Molecular Weight

278.3

Appearance

Red needle crystal

Botanical Source

Salvia miltiorrhiza,Aquilaria sinensis

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1COC2=C1C(=O)C(=O)C3=C2C=CC4=C(C=CC=C43)C

Synonyms

1,6-Dimethyl-1,2-dihydrophenanthro[1,2-b]furan-10,11-dione/1,2-dihydrotanshinone/Tanshinone I,dihydro/dihydrotanshinone 1/1,2-dihydrotanshinone I/15,16-dihydrotanshinone I/Phenanthro[1,2-b]furan-10,11-dione, 1,2-dihydro-1,6-dimethyl-/Dihydrotanshinone I

IUPAC Name

(1R)-1,6-dimethyl-1,2-dihydronaphtho[1,2-g][1]benzofuran-10,11-dione

Density

1.3±0.1 g/cm3

Solubility

Methanol; Ethyl Acetate

Flash Point

214.9±28.8 °C

Boiling Point

479.2±45.0 °C at 760 mmHg

Melting Point

214.0 to 218.0 °C

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:87205-99-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28934484

Abstract

The Human antigen R protein (HuR) is an RNA-binding protein that recognizes U/AU-rich elements in diverse RNAs through two RNA-recognition motifs, RRM1 and RRM2, and post-transcriptionally regulates the fate of target RNAs. The natural product dihydrotanshinone-I (DHTS) prevents the association of HuR and target RNAs in vitro and in cultured cells by interfering with the binding of HuR to RNA. Here, we report the structural determinants of the interaction between DHTS and HuR and the impact of DHTS on HuR binding to target mRNAs transcriptome-wide. NMR titration and Molecular Dynamics simulation identified the residues within RRM1 and RRM2 responsible for the interaction between DHTS and HuR. RNA Electromobility Shifts and Alpha Screen Assays showed that DHTS interacts with HuR through the same binding regions as target RNAs, stabilizing HuR in a locked conformation that hampers RNA binding competitively. HuR ribonucleoprotein immunoprecipitation followed by microarray (RIP-chip) analysis showed that DHTS treatment of HeLa cells paradoxically enriched HuR binding to mRNAs with longer 3’UTR and with higher density of U/AU-rich elements, suggesting that DHTS inhibits the association of HuR to weaker target mRNAs. In vivo, DHTS potently inhibited xenograft tumor growth in a HuR-dependent model without systemic toxicity.

© The Author(s) 2017. Published by Oxford University Press on behalf of Nucleic Acids Research.

Title

Regulation of HuR structure and function by dihydrotanshinone-I.

Author

Lal P1, Cerofolini L2, D'Agostino VG1, Zucal C1, Fuccio C2, Bonomo I1, Dassi E1, Giuntini S2, Di Maio D3,4, Vishwakarma V5, Preet R5, Williams SN5, Fairlamb MS5, Munk R6, Lehrmann E6, Abdelmohsen K6, Elezgarai SR7, Luchinat C2, Novellino E8, Quattrone A1, Biasini E1,7, Manzoni L9, Gorospe M6, Dixon DA5, Seneci P10, Marinelli L8, Fragai M2, Provenzani A1.

Publish date

2017 Sep 19

PMID

32200384

Abstract

INTRODUCTION:
The plaques formed by amyloid-β (Aβ) accumulation and neurofibrillary tangles formed by hyper-phosphorylated tau protein are the 2 major pathologies of Alzheimer’s disease (AD). Recently, autophagy is considered to be a self-degradation process of preserved cytoplasmic abnormal substances, including Aβ and tau.

METHODS:
α-Screen assay is used to discover a new mammalian target of rapamycin (mTOR) signaling inhibitor, and laser scanning confocal microscopic analysis is used to investigate the autophagy formation. Lastly, ELISA and Western blot assays are used to identify the mTOR signaling inhibitor effect on Aβ and tau and the underlying mechanism.

RESULTS:
In the current study, we discover that dihydrotanshinone I (DTS I), extracted from Radix Salviae, can obviously inhibit mTOR phosphorylation and increase autophagy via increasing AMPK phosphorylation. Further study demonstrates that DTS I increases Aβ clearance and decreases Tau phosphorylation through autophagy enhancement involved with AMPK/mTOR pathway.

CONCLUSION:
Our study indicates that DTS I can increase Aβ clearance and decrease Tau phosphorylation via autophagy enhancing involved with AMPK/mTOR pathway, which highlights the therapeutic potential of DTS I for the treatment of AD.

© 2020 S. Karger AG, Basel.

KEYWORDS

Alzheimer’s disease; Amyloid-β; Autophagy; Dihydrotanshinone I; Tau

Title

Dihydrotanshinone I Increase Amyloid-β Clearance and Decrease Tau Phosphorylation via Enhancing Autophagy.

Author

Bao Z1, Zhang H1, Jiao H1, Chu X2, Fu J3, Wang L1.

Publish date

2020 Mar 20

PMID

29496522

Abstract

Ulcerative colitis (UC) is a chronic and relapsing inflammatory disorder of the colon and rectum with increasing morbidity in recent years. 15,16-dihydrotanshinone Ӏ (DHT) is a natural product with multiple bioactivities. In this study, we aimed to investigate the protective effect and potential mechanisms of DHT on UC. Dextran sulfate sodium salt (DSS) was administrated in drinking water for 7 days to induce UC in mice. DHT (10 and 25 mg/kg) significantly alleviated DSS-induced body weight loss, disease activity index (DAI) scores, and improved histological alterations of colon tissues. DHT inhibited the myeloperoxidase (MPO) activity, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in colon tissues and decreased serum levels of TNF-α, IL-1β, IL-6, and high-mobility group box 1 (HMGB1). Furthermore, increased expression of kinases receptor-interacting protein 1 (RIP1), RIP3, mixed lineage kinase domain-like protein (MLKL) and decreased expression of caspase-8 in colon tissues were partially restored by DHT. In LPS-stimulated RAW264.7 macrophages, DHT significantly inhibited generation of nitric oxide, IL-6, TNF-α and protein expression of iNOS, COX-2. In addition, increased expression of iNOS, COX-2, and phosphorylated RIP1, RIP3, MLKL in response to LPS plus Z-VAD (LZ) were also suppressed by DHT. DHT had no effect on TNF-α + BV6 + Z-VAD (TBZ) induced phosphorylation of RIPs and MLKL in HT29 cells. Especially, DHT showed no effect on LZ and TBZ-induced necroptosis in RAW264.7 and HT29 cells, respectively. In summary, DHT alleviated DSS-induced UC in mice by suppressing pro-inflammatory mediators and regulating RIPs-MLKL-caspase-8 axis.

Copyright © 2018 Elsevier Inc. All rights reserved.

KEYWORDS

15,16-Dihydrotanshinone I; Inflammation; Necroptosis; Ulcerative colitis

Title

Dihydrotanshinone I, a natural product, ameliorates DSS-induced experimental ulcerative colitis in mice.

Author

Guo Y1, Wu X2, Wu Q1, Lu Y1, Shi J1, Chen X3.

Publish date

2018 Apr 1


Description :

Dihydrotanshinone I is a natural compound extracted from Salvia miltiorrhiza Bunge which has been widely used for treating cardiovascular diseases.