Tauro-β-muricholic Acid (sodium salt) is a reversible, competitive farnesyl X receptor (FXR) antagonist (IC50 = 40μM) [1]. Tauro-β-muricholic Acid competitively inhibits FXR activation, thereby interfering with the FXR-SHP and FXR-FGF15 pathways, enhancing bile acid synthesis and regulating related metabolic signaling [2-3]. Tauro-β-muricholic Acid is primarily used in cholestasis research [4].
In Ntcp-HepG2 cells, Co-culture with Tauro-β-muricholic Acid (25μM; 4h) can reduce the cell apoptosis rate to 49% [5]. In STC-1 cells, Tauro-β-muricholic Acid (100-600μM; 24h) treatment triggered a dose-dependent increase in GLP-1 secretion [6].
In Bsep−/− mice, Tauro-β-muricholic Acid (150-600nmol/min; iv; 30min, 60min) infusion increased bile salt secretion [7]. In C70-KO mice, Oral administration of Tauro-β-muricholic Acid (500mg/kg; po; 8 weeks) can reduce the incidence of chronic biliary cholangitis in mice by 40% [8].
References:
[1]. Kuribayashi H, Miyata M, Yamakawa H, et al. Enterobacteria-mediated deconjugation of taurocholic acid enhances ileal farnesoid X receptor signaling[J]. European journal of pharmacology, 2012, 697(1-3): 132-138.
[2]. Miyata M, Tanaka T, Takahashi K, et al. Cholesterol-lowering effects of taurine through the reduction of ileal FXR signaling due to the alteration of ileal bile acid composition[J]. Amino acids, 2021, 53(10): 1523-1532.
[3]. Rau M, Stieger B, Monte M J, et al. Alterations in enterohepatic Fgf15 signaling and changes in bile acid composition depend on localization of murine intestinal inflammation[J]. Inflammatory Bowel Diseases, 2016, 22(10): 2382-2389.
[4]. Zhao D S, Jiang L L, Fan Y X, et al. Identification of urine tauro-β-muricholic acid as a promising biomarker in Polygoni Multiflori Radix-induced hepatotoxicity by targeted metabolomics of bile acids[J]. Food and chemical toxicology, 2017, 108: 532-542.
[5]. Denk G U, Kleiss C P, Wimmer R, et al. Tauro-β-muricholic acid restricts bile acid-induced hepatocellular apoptosis by preserving the mitochondrial membrane potential[J]. Biochemical and biophysical research communications, 2012, 424(4): 758-764.
[6]. Xie Z, Jiang H, Liu W, et al. The triterpenoid sapogenin (2α-OH-Protopanoxadiol) ameliorates metabolic syndrome via the intestinal FXR/GLP-1 axis through gut microbiota remodelling[J]. Cell Death & Disease, 2020, 11(9): 770.
[7]. Gooijert K E R, Havinga R, Wolters H, et al. The mechanism of increased biliary lipid secretion in mice with genetic inactivation of bile salt export pump[J]. American Journal of Physiology-Gastrointestinal and Liver Physiology, 2015, 308(5): G450-G457.
[8]. Chen H, Jiang X, Li Y, et al. A Gallbladder‐Specific Hydrophobic Bile Acid‐FXR‐MUC1 Signaling Axis Mediates Cholesterol Gallstone Formation[J]. Advanced Science, 2025, 12(13): 2401956.
Tauro-β-muricholic Acid (sodium salt)是一种可逆的竞争性法尼基X受体（FXR）拮抗剂（IC50 = 40μM) [1]。Tauro-β-muricholic Acid竞争性抑制FXR活化，从而干扰FXR-SHP和FXR-FGF15通路，增强胆汁酸合成并调节相关的代谢信号传导 [2-3]。Tauro-β-muricholic Acid主要用于胆汁淤积研究 [4]。
在Ntcp-HepG2细胞中，与Tauro-β-muricholic Acid（25μM；4h）共培养可使细胞凋亡率降低至49% [5]。在STC-1细胞中，Tauro-β-muricholic Acid 100-600μM；24h）处理可引发GLP-1分泌的剂量依赖性增加 [6]。
在Bsep−/−小鼠中，输注Tauro-β-muricholic Acid（150-600nmol/min；iv；30min，60min）可增加胆汁盐的分泌 [7]。在C70-KO小鼠中，口服Tauro-β-muricholic Acid（500mg/kg；po；8周）可使小鼠慢性胆汁性胆管炎的发病率降低40% [8]。