Taurodeoxycholic acid, a bile acid, stabilizes the mitochondrial membrane, decreases free radical formation. Taurodeoxycholic acid inhibits apoptosis by blocking a calcium-mediated apoptotic pathway as well as caspase-12 activation. Taurodeoxycholic acid exhibits neuroprotective effect in 3-nitropropionic acid induced mouse model or genetic mouse model of Huntington’s disease (HD)[2].In Vitro: Taurodeoxycholic acid (50 μM, 100 μM; 4 h) increases oligonucleosomal DNA cleavage and apoptotic nuclei in primary human hepatocytes.
Taurodeoxycholic acid (400 μM; 18-24 h) increases DNA fragmentation and PARP cleavage in human liver-derived cell line Huh7 cells, thus induces apoptosis[2].
In Vivo: Taurodeoxycholic acid (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).
Taurodeoxycholic acid (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.