Taurolithocholic Acid (sodium salt) is a potent, taurine-conjugated bile acid that facilitates the absorption of lipids and sterols in the intestine[1]. Taurine-conjugated bile acids, compounds formed via amide bonds between bile acids and taurine, play a central role in emulsifying fats, maintaining cholesterol homeostasis, and regulating host metabolism[2]. Taurolithocholic Acid (sodium salt) is commonly used in research on bile acid signaling, cholestasis, and hepatobiliary/pancreatic diseases[3,4].
In vitro, treatment of freshly isolated rat hepatocytes with Taurolithocholic Acid (sodium salt) (5µM) for 5-60min resulted in a sustained and significant activation of PI3K-dependent protein kinase B (PKB/Akt), reaching 194% of the control group's activity at 60min[5]. Treatment of short-term cultured rat hepatocytes with Taurolithocholic Acid (sodium salt) (10µM) for 10min selectively induced the translocation of ε-protein kinase C (ε-PKC) to the cell membrane, increasing its membrane-bound fraction by approximately 47.9%, while showing no significant effect on the distribution of α-, δ-, or ζ-PKC isoforms[6].
In vivo, intravenous administration of Taurolithocholic Acid (sodium salt) (5-100mg/kg) to male Sprague Dawley rats induced dose-dependent cholestasis. The 100mg/kg dose nearly immediately halted bile flow after injection, with gradual recovery observed over 24-30h[7].
References:
[1] XU J, XIE S, CHI S, et al. Protective effects of taurocholic acid on excessive hepatic lipid accumulation via regulation of bile acid metabolism in grouper[J]. Food & Function, 2022, 13(5): 3050-3062.
[2] GUZIOR D V, QUINN R A. Microbial transformations of human bile acids[J]. Microbiome, 2021, 9(1): 140.
[3] DENK G U, MAITZ S, WIMMER R, et al. Conjugation is essential for the anticholestatic effect of NorUrsodeoxycholic acid in taurolithocholic acid–induced cholestasis in rat liver[J]. Hepatology, 2010, 52(5): 1758-1768.
[4] ZHANG Z, GUO X, LIU J, et al. Conjugated bile acids alleviate acute pancreatitis through inhibition of TGR5 and NLRP3 mediated inflammation[J]. Journal of Translational Medicine, 2024, 22(1): 1124.
[5] BEUERS U, DENK G U, SOROKA C J, et al. Taurolithocholic acid exerts cholestatic effects via phosphatidylinositol 3-kinase-dependent mechanisms in perfused rat livers and rat hepatocyte couplets[J]. Journal of Biological Chemistry, 2003, 278(20): 17810-17818.
[6] BEUERS U, PROBST I, SOROKA C, et al. Modulation of protein kinase C by taurolithocholic acid in isolated rat hepatocytes[J]. Hepatology, 1999, 29(2): 477-482.
[7] PRIESTLY B G, CÔTÉ M G, PLAA G L. Biochemical and morphological parameters of taurolithocholate-induced cholestasis[J]. Canadian Journal of Physiology and Pharmacology, 1971, 49(12): 1078-1091.
Taurolithocholic Acid (sodium salt)是一种强效的，可帮助吸收肠道中脂质和甾醇的牛磺酸共轭胆汁酸[1]。牛磺酸共轭胆汁酸是胆汁酸与牛磺酸通过酰胺键结合形成的化合物，在乳化脂肪、维持胆固醇稳态和调节宿主代谢等方面发挥核心作用[2]。Taurolithocholic Acid (sodium salt)通常用于胆汁酸信号转导、胆汁淤积和肝胆/胰腺相关疾病的研究[3,4]。
在体外，Taurolithocholic Acid (sodium salt)（5μM）处理离体培养的大鼠肝细胞5-60min，能持续且显著地激活PI3K依赖的蛋白激酶B（PKB/Akt），在60min时活性达到对照组的194%[5]。Taurolithocholic Acid (sodium salt)（10μM）处理离体短期培养的大鼠肝细胞10min，能选择性诱导ε-蛋白激酶C（ε-PKC）向细胞膜转位，使其膜结合部分增加约47.9%，而对α-、δ-和ζ-PKC亚型的分布无显著影响[6]。
在体内，Taurolithocholic Acid (sodium salt)（5-100mg/kg）经静脉注射给药于雄性Sprague Dawley大鼠，可诱导剂量依赖性胆汁淤积，其中100mg/kg剂量可在注射后几乎立即停止胆汁流动，并在24-30h内逐渐恢复[7]。