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Sodium Tauroursodeoxycholate (TUDC) Sale

(Synonyms: 牛磺熊去氧胆酸钠; Tauroursodeoxycholic acid sodium; TUDCA sodium; UR 906 sodium) 目录号 : GC17425

Tauroursodeoxycholate (Tauroursodeoxycholic acid; TUDCA) sodium 是一种内质网 (ER) 应激抑制剂。 Tauroursodeoxycholate 显着降低凋亡分子的表达,例如 caspase-3 和 caspase-12。 Tauroursodeoxycholate 也抑制 ERK。

Sodium Tauroursodeoxycholate (TUDC) Chemical Structure

Cas No.:35807-85-3

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥378.00
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100mg
¥504.00
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500mg
¥1,491.00
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Sample solution is provided at 25 µL, 10mM.

Description

Sodium tauroursodeoxycholate (TUDC) shows therapeutic effect on cholestasis [1, 2]. In human erythrocytes, it inhibited 2’,7’-bis-(carboxypropyl)-5(6)-carboxyfluorescein (BCPCF) efflux induced by bile salts with an IC50 value of 560 µM [3].

Cholestasis is the syndrome resulted from the impairment of the formation of bile, a vital function [4].

cVA-of-CLF means the canalicular vacuolar accumulation of cholyllysylfluorescein [1]. cVA of CLF is a parameter to indicate overall biliary secretion [5]. Incubation with 17βEG dose-dependently decreased the cVA-of-CLF in cells. 17βEG at a concentration of 50 µM decreased cVA-of-CLF by 40%. The simultaneous incubation with TUDC and 17βEG improved the decreased cVA by 24%. The simultaneous incubation with SAMe and 17βEG improved the decreased cVA by 18%. The simultaneous incubation with TUDC, SAMe and 17βEG improved the decreased cVA by 28%. But the effect of TUDC + SAMe was not significantly greater than the effect of either protectant alone [1].

In rats, intrahepatic cholestasis was induced by the administration of phalloidin at an i.p. dose of 500 µg/kg for 7 days. In these treated rats, bile flow was decreased, and activities of glutamic pyruvic transaminase, leucine aminopeptidase, serum alkaline phosphatase, and concentrations of bile acid, phospholipid and cholesterol were increased. But these effects were significantly suppressed by tauroursodeoxycholate. In these rats, excretion rates of biliary cholesterol and phospholipid were significantly improved by tauroursodeoxycholate [2].

References:
[1].  Milkiewicz P, Roma MG, Cardenas R, et al. Effect of tauroursodeoxycholate and S-adenosyl-l-methionine on 17β-estradiol glucuronide-induced cholestasis. Journal of hepatology, 2001, 34(2): 184-191.
[2].  Ishizaki K, Kinbara S, Hirabayashi N, et al. Effect of sodium tauroursodeoxycholate on phalloidin-induced cholestasis in rats. European journal of pharmacology, 2001, 421(1): 55-60.
[3].  Mrowczynska L, Bobrowska-Hgerstrand M, Wrobel A, et al. Inhibition of MRP1-mediated efflux in human erythrocytes by mono-anionic bile salts. Anticancer research, 2005, 25(5): 3173-3178.
[4].  Trauner M, Meier PJ, Boyer JL. Molecular pathogenesis of cholestasis. New England Journal of Medicine, 1998, 339(17): 1217-1227.
[5].  Milkiewicz P, Roma MG, Elias E, et al. Hepatoprotection with tauroursodeoxycholate and β muricholate against taurolithocholate induced cholestasis: involvement of signal transduction pathways. Gut, 2002, 51(1): 113-119.

实验参考方法

Cell experiment:

Cell viability and proliferation are measured using Ez-Cytox. VSMCs (5×103 cells) are seeded onto 96-well plates in Smooth Muscle Cell Growth Medium 2 (SMCGM2) and cultured. After serum starvation, Tauroursodeoxycholate (0, 50, 100, and 200 μM) is added to the hVSMCs, with or without 1,2-bis(o-aminophenoxy) ethane-N,N,N′,N′-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA, 10 μM) and 7-hydroxystaurosporine (H7, 10 μM) and cultured for 24 h. To assess the effect of Tauroursodeoxycholate on the PDGF-stimulated hVSMC proliferation, hVSMCs are seeded onto 96-well plates and cultured. After serum starvation, Tauroursodeoxycholate (0, 50, 100, and 200 μM) is added to the hVSMCs, with or without PDGF-BB (50 ng/mL) and cultured. After addition of 10 μL of Ez-Cytox into each well, cell viability is evaluated by measuring the optical density at 450 nm[1].

Animal experiment:

Rats[1]Sprague-Dawley rats are anaesthetized with a combined anaesthetic (Ketamine, 70 mg/kg; Xylazine, 7 mg/kg ip). Tauroursodeoxycholate is administered orally once a day, in different concentrations (i.e. vehicle, 10, 50, and 100 mg/kg) for 2 weeks. The carotid arteries are fixed by perfusion with 4% formaldehyde, then the tissues are embedded in paraffin, and sections (8 μm) are stained with H&E[1]. Mice[2]Thirty ApoE-/- C57BL/6 male mice aged 8 weeks are randomly divided into three groups (n=10 in each group): (i) sham operated and injected with physiologic (0.9%) saline as vehicle (normal: group); (ii) mini-osmotic pumps are implanted subcutaneously into the right flank of ApoE-/- mice to release Ang II (1000 ng/kg/min) over the course of 28 days (AAA model group); (iii) AAA model mice treated with Tauroursodeoxycholate daily for 4 weeks at a dosage of 0.5 g/kg/day in drinking water (Tauroursodeoxycholate group). Mice are sacrificed after 28 days of Ang II infusion[2].

References:

[1]. Kim SY, et al. Tauroursodeoxycholate (TUDCA) inhibits neointimal hyperplasia by suppression of ERK via PKCα-mediated MKP-1 induction. Cardiovasc Res. 2011 Nov 1;92(2):307-16.
[2]. Qin Y, et al. Tauroursodeoxycholic Acid Attenuates Angiotensin II Induced Abdominal Aortic Aneurysm Formation in Apolipoprotein E-deficient Mice by Inhibiting Endoplasmic Reticulum Stress. Eur J Vasc Endovasc Surg. 2017 Mar;53(3):337-345.

化学性质

Cas No. 35807-85-3 SDF
别名 牛磺熊去氧胆酸钠; Tauroursodeoxycholic acid sodium; TUDCA sodium; UR 906 sodium
化学名 sodium (R,Z)-4-((3R,5S,7S,8R,9S,10S,13R,14S,17R)-3,7-dihydroxy-10,13-dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)-N-(2-sulfoethyl)pentanimidate
Canonical SMILES C[C@]([C@@]1([H])CC[C@@]2([H])[C@@]([C@](O)([H])C[C@]3([H])C[C@@](O)([H])CC[C@@]34C)([H])[C@]4([H])CC[C@]12C)([H])CC/C([O-])=N/CCS(O)(=O)=O.[Na+]
分子式 C26H44NNaO6S 分子量 521.69
溶解度 ≥ 26.1mg/mL in DMSO 储存条件 Store at -20°C
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1 mM 1.9168 mL 9.5842 mL 19.1685 mL
5 mM 0.3834 mL 1.9168 mL 3.8337 mL
10 mM 0.1917 mL 0.9584 mL 1.9168 mL
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