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]。
















