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Taurocholic Acid 3-sulfate (sodium salt) Sale

(Synonyms: 3-Sulfocholyl Taurine, TCA3S) 目录号 : GC48400

A metabolite of taurocholic acid

Taurocholic Acid 3-sulfate (sodium salt) Chemical Structure

Cas No.:71781-33-4

规格 价格 库存 购买数量
500µg
¥496.00
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1mg
¥942.00
现货
5mg
¥3,975.00
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10mg
¥6,956.00
现货

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Sample solution is provided at 25 µL, 10mM.

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产品描述

Taurocholic acid 3-sulfate (TCA3S) is a metabolite of the conjugated bile acid taurocholic acid .1 Plasma levels of TCA3S are elevated in wild-type and Sortilin 1 (Sort1) knockout mice at 6 hours following bile duct ligation (BDL) and are further elevated in Sort1 knockout mice at 24 hours post-BDL.2

1.Lefebvre, P., Cariou, B., Lien, F., et al.Role of bile acids and bile acid receptors in metabolic regulationPhysiol. Rev.89(1)147-191(2009) 2.Li, J., Woolbright, B.L., Zhao, W., et al.Sortilin 1 loss-of-function protects against cholestatic liver injury by attenuating hepatic bile acid accumulation in bile duct ligated miceToxicol. Sci.161(1)34-47(2018)

Chemical Properties

Cas No. 71781-33-4 SDF
别名 3-Sulfocholyl Taurine, TCA3S
Canonical SMILES C[C@H](CCC(NCCS([O-])(=O)=O)=O)[C@@]1([H])CC[C@@]2([H])[C@]3([H])[C@H](O)C[C@]4([H])C[C@H](OS([O-])(=O)=O)CC[C@]4(C)[C@@]3([H])C[C@H](O)[C@@]21C.[Na+].[Na+]
分子式 C26H43NO10S2•2Na 分子量 639.7
溶解度 DMF: 1 mg/ml,DMSO: 0.3 mg/ml,PBS (pH 7.2): 1 mg/ml 储存条件 -20°C
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1 mg 5 mg 10 mg
1 mM 1.5632 mL 7.8162 mL 15.6323 mL
5 mM 0.3126 mL 1.5632 mL 3.1265 mL
10 mM 0.1563 mL 0.7816 mL 1.5632 mL
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Research Update

Protective effects of flavonoids from Coreopsis tinctoria Nutt. on experimental acute pancreatitis via Nrf-2/ARE-mediated antioxidant pathways

J Ethnopharmacol 2018 Oct 5;224:261-272.PMID:29870787DOI:10.1016/j.jep.2018.06.003.

Ethnopharmacological relevance: Oxidative stress is a prominent feature of clinical acute pancreatitis (AP). Coreopsis tinctoria has been used traditionally to treat pancreas disorders like diabetes mellitus in China and Portugal and its flavonoid-rich fraction contain the main phytochemicals that have antioxidant and anti-inflammatory activities. Aim of the study: To investigate the effects of flavonoids isolated from C. tinctoria on experimental AP and explore the potential mechanism. Materials and methods: LC-MS based online technique was used to analyse and isolate targeted flavonoids from C. tinctoria. Freshly isolated mouse pancreatic acinar cells were treated with taurocholic acid sodium salt hydrate (NaT, 5 mM) with or without flavonoids. Fluorescence microscopy and a plate reader were used to determine necrotic cell death pathway activation (propidium iodide), reactive oxygen species (ROS) production (H2-DCFDA) and ATP depletion (luminescence) where appropriate. AP was induced by 7 repeated intraperitoneal caerulein injections (50 μg/kg) at hourly interval in mice or retrograde infusion of taurolithocholic acid 3-sulfate disodium salt (TLCS; 5 mM, 50 μL) into the pancreatic duct in mice or infusion of NaT (3.5%, 1 mL/kg) in rats. A flavonoid was intraperitoneally administered at 0, 4, and 8 h after the first caerulein injection or post-operation. Disease severity, oxidative stress and antioxidant markers were determined. Results: Total flavonoids extract and flavonoids 1-6 (C1-C6) exhibited different capacities in reducing necrotic cell death pathway activation with 0.5 mM C1, (2 R,3 R)-taxifolin 7-O-β-D-glucopyranoside, having the best effect. C1 also significantly reduced NaT-induced ROS production and ATP depletion. C1 at 12.5 mg/kg and 8.7 mg/kg (equivalent to 12.5 mg/kg for mice) significantly reduced histopathological, biochemical and immunological parameters in the caerulein-, TLCS- and NaT-induced AP models, respectively. C1 administration increased pancreatic nuclear factor erythroid 2-related factor 2 (Nrf2) and Nrf2-medicated haeme oxygenase-1 expression and elevated pancreatic antioxidant enzymes superoxide dismutase and glutathione peroxidase levels. Conclusions: Flavonoid C1 from C. tinctoria was protective in experimental AP and this effect may at least in part be attributed to its antioxidant effects by activation of Nrf2-mediated pathways. These results suggest the potential utilisation of C. tinctoria to treat AP.