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Tauroursodeoxycholate (TUDCA) Sale

(Synonyms: 牛磺熊去氧胆酸; Tauroursodeoxycholic acid; TUDCA; UR 906) 目录号 : GC34181

牛磺酸脱氧胆酸盐(TUDCA)是包括肝细胞在内的多种细胞的细胞保护剂,也是癌症细胞凋亡的诱导剂。牛磺酸脱氧胆酸盐作为一种内质网应激抑制剂,通过减少内质网应激,有效地保护肝细胞和恢复葡萄糖稳态。.

Tauroursodeoxycholate (TUDCA) Chemical Structure

Cas No.:14605-22-2

规格 价格 库存 购买数量
50mg
¥500.00
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实验参考方法

Cell experiment [1]:

Cell lines

Hepatocytes and HuH‐NTCP cells

Preparation Method

Hepatocytes and HuH‐NTCP cells were treated with DMSO (Con), 100 µmol/L CPT‐cAMP (cAMP) for 15 min, 10 µmol/L TLC for 25 min, 100 µmol/L CPT‐cAMP + 10 µmol/L TLC for 25 min, or 25 µmol/L TUDC for 15 min or 10 µmol/L TLC for 25 min or 25 µmol/L TUDC + 10 µmol/L TLC for 25 min.

Reaction Conditions

25 µmol/L; 25 min

Applications

Cyclic AMP and TUDC inhibit TLC‐induced increases in plasma membrane PKC ε in rat hepatocytes. Cyclic AMP and TUDC inhibit TLC‐induced increases in plasma membrane PKC ε in HuH‐NTCP cells.

Animal experiment [2]:

Animal models

TNBS(2,4,6-trinitrobenzene sulfonic acid)-induced ulcerative colitis in mice

Preparation Method

After the induction of colitis for 24h, the mice were administrated orally with tauroursodeoxycholate (20, 40 and 60mg/kg) and sulfasalazine (500mg/kg) by gavage for 7 consecutive days. The inhibition effects were evaluated by the body of weight change, survival rate, macroscopical and histological evaluations.

Dosage form

20, 40 and 60mg/kg; p.o.

Applications

Treatment with different doses of tauroursodeoxycholate (20, 40 and 60mg/kg) significantly improved the body weight change, decreased the macroscopic and histopathological scores. Compared with the model group, the accumulation of MPO activity, the colonic tissue levels of IL-1β, IFN-γ and TNF-α were significantly reduced in the tauroursodeoxycholate treated groups. Moreover, tauroursodeoxycholate assuaged the symptoms of colitis.

References:

[1] Park SW, et al. Mechanism of inhibition of taurolithocholate-induced retrieval of plasma membrane MRP2 by cyclic AMP and tauroursodeoxycholate. Physiol Rep. 2017 Dec;5(23):e13529.
[2] Yang Y, et al. Tauroursodeoxycholate improves 2,4,6-trinitrobenzenesulfonic acid-induced experimental acute ulcerative colitis in mice. Int Immunopharmacol. 2016 Jul;36:271-276.

产品描述

Tauroursodeoxycholate (TUDCA) is a cytoprotective agent in a variety of cells including hepatocytes as well as an inducer of apoptosis in cancer cells[1]. Tauroursodeoxycholate, as an endoplasmic reticulum (ER) stress inhibitor, is effective in protecting the hepatocytes and restoring glucose homeostasis by reducing the endoplasmic reticulum stress[2].

In vitro, 200 µM TUDCA suppressed viability of hVSMCs (vascular smooth muscle cells) by inhibition of ERK (extracellular signal-regulated kinase) phosphorylation, through induction of MKP-1 (MAPK phosphatase-1) via PKCα (protein kinase Cα). And TUDCA inhibited both the proliferation and migration of PDGF-stimulated hVSMCs[1]. In vitro, 25 µM Tauroursodeoxycholate (TUDC) increases plasma membrane multidrug resistance-associated protein 2 (MRP2). And TUDC and cAMP increase Rab11 activity[3].

In vivo, TUDCA prevents the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-dependent decrease of dopaminergic fibers and ATP levels, mitochondrial dysfunction and neuroinflammation. TUDCA administration (50 mg/kg), the mice also displayed reduction in foot dragging and an overall improvement in gait[4]. Mice were treated with TUDCA 0.5 mg/g every 3 days, for a total of 7 injections, which showed an increase in neuromuscular junction innervation in the mutated mice[5]. TUDCA treatment (100 mg, 3 times/day) also reduces neurological impairment in rats with acute cerebral infarction[6].

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.

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.

Park SW, et al. Rab11, but not Rab4, facilitates cyclic AMP- and tauroursodeoxycholate-induced MRP2 translocation to the plasma membrane. Am J Physiol Gastrointest Liver Physiol. 2014 Oct 15;307(8):G863-70.

[3] Rosa AI, et al. Tauroursodeoxycholic acid improves motor symptoms in a mouse model of Parkinson's disease. Mol Neurobiol. 2018;55(12):9139-9155.

[4] Thams S, et al. A stem cell-based screening platform identifies compounds that desensitize motor neurons to endoplasmic reticulum stress. Mol Ther. 2019;27(1):87-101.

[5] Bian KY, et al. DCA can improve the ACI-induced neurological impairment through negative regulation of Nrf2 signaling pathway. Eur Rev Med Pharmacol Sci. 2019;23(1):343-351.

References:

牛磺酸脱氧胆酸盐(TUDCA)是包括肝细胞在内的多种细胞的细胞保护剂,也是癌症细胞凋亡的诱导剂[1]。牛磺酸脱氧胆酸盐作为一种内质网应激抑制剂,通过减少内质网应激,有效地保护肝细胞和恢复葡萄糖稳态[2]。

在体外,200µM TUDCA通过抑制ERK(细胞外信号调节激酶)磷酸化,通过PKCα(蛋白激酶Cα)诱导MKP-1(MAPK磷酸酶-1),抑制hVSMCs(血管平滑肌细胞)的活力。TUDCA同时抑制PDGF刺激的hVSMCs的增殖和迁移[1]。在体外,25µM牛磺酸脱氧胆酸盐(TUDC)可增加质膜多药耐药相关蛋白2(MRP2)。TUDC和cAMP可提高Rab11活性[3]。

在体内,TUDCA可防止MPTP(1-甲基-4-苯基-1,2,3,6-四氢吡啶)依赖性多巴胺能纤维和ATP水平的降低、线粒体功能障碍和神经炎症。给予TUDCA(50 mg/kg)后,小鼠的拖脚能力也有所减少,步态也有所改善[4]。每3天用TUDCA 0.5 mg/g治疗小鼠,共注射7次,这表明突变小鼠的神经肌肉接头神经支配增加[5]。TUDCA治疗(100 mg,3次/天)也可减少急性脑梗死大鼠的神经损伤[6]。

Chemical Properties

Cas No. 14605-22-2 SDF
别名 牛磺熊去氧胆酸; Tauroursodeoxycholic acid; TUDCA; UR 906
Canonical SMILES C[C@H](CCC(NCCS(=O)(O)=O)=O)[C@H]1CC[C@@]2([H])[C@]3([H])[C@@H](O)C[C@]4([H])C[C@H](O)CC[C@]4(C)[C@@]3([H])CC[C@]12C
分子式 C26H45NO6S 分子量 499.7
溶解度 Water:12.5mg/mL(25.02 mM) 储存条件 Store at RT
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1 mM 2.0012 mL 10.006 mL 20.012 mL
5 mM 0.4002 mL 2.0012 mL 4.0024 mL
10 mM 0.2001 mL 1.0006 mL 2.0012 mL
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Research Update

The bile acid TUDCA and neurodegenerative disorders: An overview

Life Sci 2021 May 1;272:119252.PMID:33636170DOI:10.1016/j.lfs.2021.119252.

Bear bile has been used in Traditional Chinese Medicine for thousands of years due to its therapeutic potential and clinical applications. The tauroursodeoxycholic acid (TUDCA), one of the acids found in bear bile, is a hydrophilic bile acid and naturally produced in the liver by conjugation of taurine to ursodeoxycholic acid (UDCA). Several studies have shown that TUDCA has neuroprotective action in several models of neurodegenerative disorders (ND), including Alzheimer's disease, Parkinson's disease, and Huntington's disease, based on its potent ability to inhibit apoptosis, attenuate oxidative stress, and reduce endoplasmic reticulum stress in different experimental models of these illnesses. Our research extends the knowledge of the bile acid TUDCA actions in ND and the mechanisms and pathways involved in its cytoprotective effects on the brain, providing a novel perspective and opportunities for treatment of these diseases.

Tauroursodeoxycholate-Bile Acid with Chaperoning Activity: Molecular and Cellular Effects and Therapeutic Perspectives

Cells 2019 Nov 20;8(12):1471.PMID:31757001DOI:10.3390/cells8121471.

Tauroursodeoxycholic acid (TUDCA) is a naturally occurring hydrophilic bile acid that has been used for centuries in Chinese medicine. Chemically, TUDCA is a taurine conjugate of ursodeoxycholic acid (UDCA), which in contemporary pharmacology is approved by Food and Drug Administration (FDA) for treatment of primary biliary cholangitis. Interestingly, numerous recent studies demonstrate that mechanisms of TUDCA functioning extend beyond hepatobiliary disorders. Thus, TUDCA has been demonstrated to display potential therapeutic benefits in various models of many diseases such as diabetes, obesity, and neurodegenerative diseases, mostly due to its cytoprotective effect. The mechanisms underlying this cytoprotective activity have been mainly attributed to alleviation of endoplasmic reticulum (ER) stress and stabilization of the unfolded protein response (UPR), which contributed to naming TUDCA as a chemical chaperone. Apart from that, TUDCA has also been found to reduce oxidative stress, suppress apoptosis, and decrease inflammation in many in-vitro and in-vivo models of various diseases. The latest research suggests that TUDCA can also play a role as an epigenetic modulator and act as therapeutic agent in certain types of cancer. Nevertheless, despite the massive amount of evidence demonstrating positive effects of TUDCA in pre-clinical studies, there are certain limitations restraining its wide use in patients. Here, molecular and cellular modes of action of TUDCA are described and therapeutic opportunities and limitations of this bile acid are discussed.

UDCA, NorUDCA, and TUDCA in Liver Diseases: A Review of Their Mechanisms of Action and Clinical Applications

Handb Exp Pharmacol 2019;256:237-264.PMID:31236688DOI:10.1007/164_2019_241.

Bile acids (BAs) are key molecules in generating bile flow, which is an essential function of the liver. In the last decades, there have been great advances in the understanding of BA physiology, and new insights have emerged regarding the role of BAs in determining cell damage and death in several liver diseases. This new knowledge has helped to better delineate the pathophysiology of cholestasis and the adaptive responses of hepatocytes to cholestatic liver injury as well as of the mechanisms of injury of biliary epithelia. In this context, therapeutic approaches for liver diseases using hydrophilic BA (i.e., ursodeoxycholic acid, tauroursodeoxycholic, and, more recently, norursodeoxycholic acid), have been revamped. In the present review, we summarize current experimental and clinical data regarding these BAs and its role in the treatment of certain liver diseases.

Tauroursodeoxycholate (TUDCA) inhibits neointimal hyperplasia by suppression of ERK via PKCα-mediated MKP-1 induction

Cardiovasc Res 2011 Nov 1;92(2):307-16.PMID:21840882DOI:10.1093/cvr/cvr219.

Aims: Hyperplasia of vascular smooth muscle cells (VSMCs) after blood vessel injury is one of the major pathophysiological mechanisms associated with neointima. Tauroursodeoxycholate (TUDCA) is a cytoprotective agent in a variety of cells including hepatocytes as well as an inducer of apoptosis in cancer cells. In this study, we investigated whether TUDCA could prevent neointimal hyperplasia by suppressing the growth and migration of VSMCs. Methods and results: Transporters of TUDCA uptake in human VSMCs (hVSMCs) were analysed by RT-PCR and western blot. A knock-down experiment using specific si-RNA revealed that TUDCA was incorporated into hVSMCs via organic anion transporter 2 (OATP2). TUDCA reduced the viability of hVSMCs, which were mediated by inhibition of extracellular signal-regulated kinase (ERK) by induction of mitogen-activated protein kinase phosphatase-1 (MKP-1) via protein kinase Cα (PKCα). The anti-proliferative effect of TUDCA was reversed by treatment with 7-hydroxystaurosporine, an inhibitor of PKC, and by the knock-down of MKP-1. In addition, TUDCA suppressed hVSMC migration, which was mediated by reduced matrix metalloproteinase-9 (MMP-9) expression by ERK inhibition, as well as reduced viability of hVSMCs. Rats with carotid artery balloon injury received oral administration of TUDCA; this reduced the increase in ERK and MMP-9 caused by balloon injury. TUDCA significantly decreased the ratio of intima to media by reducing proliferation and inducing apoptosis of the VSMCs. Conclusion: TUDCA inhibits neointimal hyperplasia by reducing proliferation and inducing apoptosis of smooth muscle cells by suppression of ERK via PKCα-mediated MKP-1 induction.

Tauroursodeoxycholate (TUDCA), chemical chaperone, enhances function of islets by reducing ER stress

Biochem Biophys Res Commun 2010 Jul 9;397(4):735-9.PMID:20541525DOI:10.1016/j.bbrc.2010.06.022.

The exposure to acute or chronic endoplasmic reticulum (ER) stress has been known to induce dysfunction of islets, leading to apoptosis. The reduction of ER stress in islet isolation for transplantation is critical for islet protection. In this study, we investigated whether Tauroursodeoxycholate (TUDCA) could inhibit ER stress induced by thapsigargin, and restore the decreased glucose stimulation index of islets. In pig islets, thapsigargin decreased the insulin secretion by high glucose stimulation in a time-dependent manner (1h, 1.35+/-0.16; 2h, 1.21+/-0.13; 4h, 1.17+/-0.16 vs. 0h, 1.81+/-0.15, n=4, p<0.05, respectively). However, the treatment of TUDCA restored the decreased insulin secretion index induced by thapsigargin (thapsigargin, 1.25+/-0.12 vs. thapsigargin+TUDCA, 2.13+/-0.19, n=5, p<0.05). Furthermore, the culture of isolated islets for 24h with TUDCA significantly reduced the rate of islet regression (37.4+/-5.8% vs. 14.5+/-6.4%, n=12, p<0.05). The treatment of TUDCA enhanced ATP contents in islets (27.2+/-3.2pmol/20IEQs vs. 21.7+/-2.8pmol/20IEQs, n=9, p<0.05). The insulin secretion index by high glucose stimulation is also increased by treatment of TUDCA (2.42+/-0.15 vs. 1.92+/-0.12, n=12, p<0.05). Taken together, we suggest that TUDCA could be a useful agent for islet protection in islet isolation for transplantation.