Taurodeoxycholic acid

Taurodeoxycholate sodium salt is a bile salt-related anionic detergent. Taurodeoxycholic acid is formed in the liver by conjugation of deoxycholate with Taurine (HY-B0351). Taurodeoxycholic acid is used for isolation of membrane proteins including inner mitochondrial membrane proteins. Taurodeoxycholic acid (TDCA) exhibits anti-inflammatory and neuroprotective effects^{[1][2][3][9][10]}. In Vitro: Taurodeoxycholic acid (Taurodeoxycholic acid form) shows agonist activity at human TGR5 expressed in CHO cells by luciferase assay, with an EC₅₀ of 0.79 μM^[4].
Taurodeoxycholic acid (Taurodeoxycholic acid form, 16 h) shows agonist activity at wild type and Y89A mutant human TGR5 expressed in HEK293 cells assessed as rise in intracellular cAMP level, with EC₅₀s of 0.68 and 8.9 μM, respectively^[5].
Taurodeoxycholic acid (Taurodeoxycholic acid form, 50 μM, 100 μM; 4 h) increases oligonucleosomal DNA cleavage and apoptotic nuclei in primary human hepatocytes^[6].
Taurodeoxycholic acid (Taurodeoxycholic acid form, 400 μM, 18-24 h) increases DNA fragmentation and PARP cleavage in human liver-derived cell line Huh7 cells, thus induces apoptosis^[8].
Taurodeoxycholic acid (0.05-1.00 mM; 1-6 days) stimulates intestinal epithelial cell proliferation^[8].
Taurodeoxycholic acid (0.05-1.00 mM; 24 h) induces a significant increase in S-phase concentration and a significant decrease in G1-phase concentration of the cell cycle, increases c-myc protein and mRNA expression in IEC-6 cells^[8].
Taurodeoxycholic acid (25-400 ng/mL, with a four-fold dilution, 3 h) inhibits the activation of NF-κB in lipopolysaccharide-activated bone marrow-derived macrophages (BMDMs) by activating the cAMP-PKA axis^[9].
In Vivo: Taurodeoxycholic acid (1.25-5 mg/kg, p.o., 6 days) ameliorates dextran sodium sulfate (DSS)-induced colitis in mice^[9].
Taurodeoxycholic acid (Taurodeoxycholic acid form, 50 mg/kg; i.p.; once daliy for 34 d) prevents neuropathology and associated behavioral deficits in the 3-nitropropionic acid rat model of Huntington's disease (HD) ^[10].
Taurodeoxycholic acid (Taurodeoxycholic acid form, 500 mg/kg; s.c.; once every 3 d for 7 weeks) leads to a significant reduction in striatal neuropathology of the R6/2 transgenic HD mouse^[11].
Taurodeoxycholic acid (0.5 mg/kg; i.v., once) confers protection to C57BL/6N mice with sepsis, but does not protect TGR5 KO mice under sepsis^[12].