Taurochenodeoxycholic Acid (sodium salt)
(Synonyms: 牛磺鹅去氧胆酸钠盐; 12-Deoxycholyltaurine sodium) 目录号 : GC44992
Taurochenodeoxycholic Acid (sodium salt)是一种内源性亲水性胆汁酸，是由胆汁酸中的天然成分熊去氧胆酸（UDCA）在肝脏中与氨基酸牛磺酸进行化学结合形成的。Taurochenodeoxycholic Acid (sodium salt)已被批准用于治疗肝脏疾病。Taurochenodeoxycholic Acid (sodium salt)可以减少活性氧的形成，防止线粒体功能障碍，并降低细胞凋亡的阈值。
Cas No.:6009-98-9
Sample solution is provided at 25 µL, 10mM.
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Taurochenodeoxycholic Acid (sodium salt) is an endogenous hydrophilic bile salt that is formed by the chemical conjugation of the naturally occurring bile acid ursodeoxycholic acid (UDCA) with the amino acid taurine in the liver. Taurochenodeoxycholic Acid (sodium salt) has been approved for the treatment of liver diseases. Taurochenodeoxycholic Acid (sodium salt) can reduce the formation of reactive oxygen species, prevent mitochondrial dysfunction, and lower the threshold for cell apoptosis[1].
In vitro, Taurochenodeoxycholic Acid (sodium salt) (100μM) significantly alleviates the senescence phenotypes of mouse embryonic fibroblasts (MEFs)[2]. Taurochenodeoxycholic Acid (sodium salt) (0, 10, 100, 250 and 500μM; 7 or 20 days) enhances osteogenic differentiation through the EGFR/p-Akt/CREB1 pathway in mesenchymal stem cells[3].
In vivo, Taurochenodeoxycholic Acid (sodium salt) (400mg/kg/day; 3 weeks; i.p.) can prevent the development of glomerular and proximal tubular injury caused by a high-salt diet in ETB receptor–deficient rats, reducing renal cell death and renal cortical inflammation[1]. Taurochenodeoxycholic Acid (sodium salt) (50mg/kg; 4 months; p.o.) treatment eliminated kidney injuries induced by Col4a3 mutation in mice[4]. Taurochenodeoxycholic Acid (sodium salt) (1000mg/kg; 4 weeks; p.o.) attenuates the progression of HFD-induced non-alcoholic fatty liver disease (NAFLD) in mice[5].
References:
[1] De Miguel C, Sedaka R, Kasztan M, et al. Taurochenodeoxycholic Acid (TUDCA) abolishes chronic high salt-induced renal injury and inflammation. Acta Physiol (Oxf). 2019 May;226(1):e13227.
[2] Liu JY, Wang Y, Guo Y, et al. Taurochenodeoxycholic Acid targets HSP90 to promote protein homeostasis and extends healthy lifespan. Sci China Life Sci. 2025 Feb;68(2):416-430.
[3] Kang H, Yang S, Lee J. Taurochenodeoxycholic Acid Enhances Osteogenic Differentiation through EGFR/p-Akt/CREB1 Pathway in Mesenchymal Stem Cells. Cells. 2023 May 24;12(11):1463.
[4] Yu S, Gu X, Zheng Q, et al. Taurochenodeoxycholic Acid ameliorates renal injury induced by COL4A3 mutation. Kidney Int. 2024 Sep;106(3):433-449.
[5] Wang W, Zhao J, Gui W, et al. Taurochenodeoxycholic Acid inhibits intestinal inflammation and barrier disruption in mice with non-alcoholic fatty liver disease. Br J Pharmacol. 2018 Feb;175(3):469-484.
Taurochenodeoxycholic Acid (sodium salt)是一种内源性亲水性胆汁酸，是由胆汁酸中的天然成分熊去氧胆酸（UDCA）在肝脏中与氨基酸牛磺酸进行化学结合形成的。Taurochenodeoxycholic Acid (sodium salt)已被批准用于治疗肝脏疾病。Taurochenodeoxycholic Acid (sodium salt)可以减少活性氧的形成，防止线粒体功能障碍，并降低细胞凋亡的阈值[1]。
在体外实验中，Taurochenodeoxycholic Acid (sodium salt)（100μM）显著减轻了小鼠胚胎成纤维细胞（MEFs）的衰老表型[2]。Taurochenodeoxycholic Acid (sodium salt)（0, 10, 100, 250和500μM; 7天或20天）通过EGFR/p-Akt/CREB1信号通路增强间充质干细胞的成骨分化[3]。
在体内实验中，Taurochenodeoxycholic Acid (sodium salt)（400mg/kg/天; 3周; 腹腔注射）可以预防高盐饮食在ETB受体缺陷大鼠中引起的肾小球和近曲小管损伤的发展，减少肾细胞死亡和肾皮质炎症[1]。Taurochenodeoxycholic Acid (sodium salt)（50mg/kg; 4个月; 口服）治疗消除了Col4a3基因突变小鼠的肾脏损伤[4]。Taurochenodeoxycholic Acid (sodium salt)（1000mg/kg; 4周; 口服）减轻了高脂饮食诱导的小鼠非酒精性脂肪性肝病（NAFLD）的进展[5]。
| Cell experiment [1]: | |
Cell lines | hMSCs |
Preparation Method | Alkaline Phosphatase (ALP) Activity Assay Cells were seeded at a density of 5 × 10³ cells per well in a 96-well plate and treated with different concentrations of Taurochenodeoxycholic Acid (sodium salt) (0, 10, 100, 250 and 500μM). After 7 days, the 96-well plate was washed twice with phosphate-buffered saline. The cells were resuspended in 0.1% Triton X-100 and incubated at 4°C for 1h. The absorbance of the cell lysate was measured at 405nm in a reaction with p-nitrophenyl phosphate, and ALP activity was calculated using a standard formula. Protein quantification of cell lysates was performed using a TCA assay kit. The amount of p-nitrophenyl phosphate was normalized to the total amount of protein and recorded as nM/μg protein. Calcium Accumulation Measurement Calcium accumulation was analyzed using alizarin red-sulfate (AR-S) staining. Cells were seeded at a density of 5×10³ cells per well in a 96-well plate and continuously cultured in Taurochenodeoxycholic Acid (sodium salt) for 20 days. The cells were then fixed with 70% (v/v) ethanol for 1h at 4°C and stained with a 40mM AR-S solution. Cells were observed under a microscope at 2.5× magnification and solubilized using 10% (w/v) cetylpyridinium chloride in 10mM sodium phosphate (pH 7.0). The absorbance was measured at 562nm using a microplate reader. |
Reaction Conditions | 0, 10, 100, 250 and 500μM; 7 or 20 days |
Applications | Taurochenodeoxycholic Acid (sodium salt) enhances osteogenic differentiation through the EGFR/p-Akt/CREB1 pathway in mesenchymal stem cells. |
| Animal experiment [2]: | |
Animal models | Ten-to-twelve week old male ETB-deficient rats (specifically, DBH-ETB;ETBsl/sl rats) and their DBH-ETB;ETB+/+ transgenic littermates (TG control rats) |
Preparation Method | Rats were randomly assigned to either a normal salt diet (0.8% NaCl) or a high salt diet (8% NaCl) for 3 weeks. The group of rats receiving the high salt diet was further divided into two subgroups, which received daily intraperitoneal injections of Taurochenodeoxycholic Acid (sodium salt) (TUDCA, 400mg/kg/day) or vehicle (isotonic saline) throughout the 3-week period. On the last day of the study (after one day of acclimatization to metabolic cages), urine was collected, a plasma sample was obtained, the animals were sacrificed, and the kidneys were harvested. In some cases, the kidneys were divided into renal cortex and outer medulla, snap-frozen in liquid nitrogen, and stored at -80℃ until further analysis. Other kidneys were fixed overnight in formalin and embedded in paraffin for immunohistochemistry studies. Since preliminary studies revealed no changes in the outer medulla, the present study focused primarily on the renal cortex. In a second set of animals, PA-C40 transmitters were implanted into the abdominal aorta to monitor blood pressure in the conscious state, as previously described. Briefly, rats were anesthetized with 2–3% isoflurane, the abdominal aorta was exposed, and the transmitter was implanted and secured with tissue glue. Animals recovered from surgery for one week before the start of the 3-week protocol, during which mean arterial pressure (MAP) was recorded at 10-sec intervals every 10min. |
Dosage form | 400mg/kg/day; 3 weeks; i.p. |
Applications | Taurochenodeoxycholic Acid (sodium salt) can prevent the development of glomerular and proximal tubular injury caused by a high-salt diet in ETB receptor–deficient rats, reducing renal cell death and renal cortical inflammation. |
References: | |
| Cas No. | 6009-98-9 | SDF | |
| 别名 | 牛磺鹅去氧胆酸钠盐; 12-Deoxycholyltaurine sodium | ||
| 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](O)CC[C@]4(C)[C@@]3([H])CC[C@@]21C.[Na+] | ||
| 分子式 | C26H44NO6S•Na | 分子量 | 521.7 |
| 溶解度 | DMF: 25 mg/ml,DMSO: 20 mg/ml,Ethanol: 2 mg/ml,PBS (pH 7.2): 3 mg/ml | 储存条件 | Store at -20°C |
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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.9168 mL | 9.5841 mL | 19.1681 mL |
| 5 mM | 0.3834 mL | 1.9168 mL | 3.8336 mL |
| 10 mM | 0.1917 mL | 0.9584 mL | 1.9168 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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2.
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Quality Control & SDS
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- Purity: >98.00%
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