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Taurochenodeoxycholic Acid

$58

  • Brand : BIOFRON

  • Catalogue Number : BD-D1226

  • Specification : 98%(HPLC)

  • CAS number : 516-35-8

  • Formula : C26H45NO6S

  • Molecular Weight : 499.7

  • PUBCHEM ID : 387316

  • Volume : 20MG

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Catalogue Number

BD-D1226

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

499.7

Appearance

White crystal

Botanical Source

Structure Type

Category

Standards;Natural Pytochemical;API

SMILES

CC(CCC(=O)NCCS(=O)(=O)O)C1CCC2C1(CCC3C2C(CC4C3(CCC(C4)O)C)O)C

Synonyms

Chenyltaurine/2-{[(3α,5β,7α,8ξ,9ξ,14ξ)-3,7-Dihydroxy-24-oxocholan-24-yl]amino}ethanesulfonic acid/Chenodeoxycholyltaurine/Chenodeoxytaurocholic acid/12-Deoxycholyltaurine/Ethanesulfonic acid, 2-[[(3α,5β,7α,8ξ,9ξ,14ξ)-3,7-dihydroxy-24-oxocholan-24-yl]amino]-/Chenodeoxycholoyltaurine/[3H]-Chenodeoxycholyltaurine/Taurochenodeoxycholic acid/12-Desoxycholyltaurine/Taurochenodesoxycholic acid

IUPAC Name

2-[[(4R)-4-[(3R,5S,7R,8R,9S,10S,13R,14S,17R)-3,7-dihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoyl]amino]ethanesulfonic acid

Applications

Taurochenodeoxycholic acid is one of the main bioactive substances of animals' bile acid

Density

1.2±0.1 g/cm3

Solubility

DMSO : ≥ 25 mg/mL (50.03 mM);

Flash Point

Boiling Point

Melting Point

InChl

InChI=1S/C26H45NO6S/c1-16(4-7-23(30)27-12-13-34(31,32)33)19-5-6-20-24-21(9-11-26(19,20)3)25(2)10-8-18(28)14-17(25)15-22(24)29/h16-22,24,28-29H,4-15H2,1-3H3,(H,27,30)(H,31,32,33)/t16-,17+,18-,19-,20+,21+,22-,24+,25+,26-/m1/s1

InChl Key

BHTRKEVKTKCXOH-BJLOMENOSA-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#:516-35-8) 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

31767094

Abstract

Pseudorabies virus (PRV) infection causes great economic losses in the pig industry. By disrupting the homeostasis of the endoplasmic reticulum (ER), many viral infections induce ER stress and trigger the unfolded protein response (UPR). However, the roles of ER stress and UPR in PRV infection remain unclear. In the present study, we demonstrate that the expression of the ER stress marker glucose-regulated protein 78 (GRP78) increased during the early stages of PRV infection, indicating that ER stress was induced. Examination of the three branches of the UPR revealed that the IRE1-XBP1 and eIF2α-ATF4 pathways were activated during PRV infection. In addition, PRV induced apoptosis in later stages of infection through the CHOP-Bcl2 axis. Overexpression of GRP78 or ER stress inducer treatment with thapsigargin could enhance PRV production. Conversely, ER stress inhibitor treatment with tauroursodeoxycholic acid reduced PRV replication. Taken together, our results reveal that PRV infection induces ER stress and activates the IRE1-XBP1 and eIF2α-ATF4 pathways.

Copyright © 2019 Elsevier B.V. All rights reserved.

KEYWORDS

ER stress; GRP78; IRE1; PRV; UPR; XBP1

Title

Induction of the unfolded protein response (UPR) during pseudorabies virus infection.

Author

Yang S1, Zhu J1, Zhou X1, Wang H1, Li X1, Zhao A2.

Publish date

2019 Dec

PMID

31387173

Abstract

Inherited retinal degeneration (RD) comprises a heterogeneous group of retinopathies that rank among the main causes of blindness. Tauroursodeoxycholic acid (TUDCA) is taurine conjugate hydrophilic bile acid that demonstrates profound protective effects against a series of neurodegenerative diseases related to oxidative stress. This study sought to evaluate the TUDCA induced effects of on a pharmacologically induced RD animal model by electroretinogram (ERG) examination, behavior tests, morphological analysis and immunochemistry assay. Massive photoreceptor degeneration in mice retina was induced by an intraperitoneal administration of N-methyl-N-nitrosourea(MNU). Subcutaneous delivery of TUDCA inhibits effectively the photoreceptor loss and visual impairments in the MNU administered mice. In the retinal flat-mounts of TUDCA treated mice, the cone photoreceptors were efficiently preserved. Furthermore, the multi-electrodes array (MEA) was used to detect the firing activities of retinal ganglion cells within the inner retinal circuits. TUDCA therapy could restrain the spontaneous firing response, enhance the light induced firing response, and preserve the basic configurations of ON-OFF signal pathway in degenerative retinas. Our MEA assay provided an example to evaluate the potency of pharmacological compounds on retinal plasticity. TUDCA affords these protective effects by modulating apoptosis and alleviating oxidative stress in the degenerative retina. In conclusion, TUDCA therapy can ameliorate the photoreceptor degeneration and rectify the abnormities in visual signal transmission. These findings suggest that TUDCA might act as a potential medication for these retinopathies with progressive photoreceptor degeneration.

Copyright © 2019 Tangdu Hospital, Fourth Military Medical University. Published by Elsevier Masson SAS.. All rights reserved.

KEYWORDS

Neurodegeneration; Photoreceptor; Retina; Therapeutics; Visual function

Title

Subcutaneous delivery of tauroursodeoxycholic acid rescues the cone photoreceptors in degenerative retina: A promising therapeutic molecule for retinopathy.

Author

Tao Y1, Dong X2, Lu X1, Qu Y3, Wang C4, Peng G5, Zhang J6.

Publish date

2019 Sep;

PMID

31254957

Abstract

Neonatal necrotizing enterocolitis (NEC) is a life-threatening disease with severe inflammation and intestinal cell apoptosis. Tauroursodeoxycholic acid (TUDCA) is a recognized endoplasmic reticulum stress (ERS) inhibitor which can inhibit cell apoptosis. Recently, intestinal cell apoptosis has been demonstrated to be vital for the pathogenesis of NEC. The purpose of the present study was to investigate the potential of TUDCA in the treatment of NEC and the possible mechanisms in vivo and in vitro. Our results showed that TUDCA reduced mortality rates, prolonged survival times, significantly diminished intestinal damage, and inhibited intestinal inflammation in the mouse model of NEC. The protective effect of TUDCA on the NEC mouse model was realized through inhibiting the expression levels of ERS markers and inhibiting the apoptosis of intestinal cells. In addition, TUDCA increased the expression of phospho-Akt (p-Akt). Furthermore, we confirmed that TUDCA inhibited the apoptosis of intestinal cells by modulating the PERK-eIF2α ERS pathway and the Akt pathway in vitro studies. Besides, TUDCA effects were impaired by AKT specific inhibitor MK2206 in vitro studies. Therefore, these results indicated that TUDCA alleviated intestinal injury in a mouse model of NEC and inhibited ERS-mediated intestinal cell apoptosis by activating the Akt pathway.

Copyright © 2019 Elsevier B.V. All rights reserved

KEYWORDS

Akt signal pathway; Apoptosis; ER stress; Necrotizing enterocolitis; Tauroursodeoxycholic acid

Title

TUDCA attenuates intestinal injury and inhibits endoplasmic reticulum stress-mediated intestinal cell apoptosis in necrotizing enterocolitis.

Author

Li P1, Fu D1, Sheng Q1, Yu S1, Bao X2, Lv Z3.

Publish date

2019 Sep