Taurodeoxycholic acid sodium hydrate (Sodium taurodeoxycholate monohydrate) prevents apoptosis by blocking a calcium-mediated apoptotic pathway as well as caspase-12 activation. Taurodeoxycholic acid sodium hydrate is investigated for use in several conditions such as Primary Biliary Cirrhosis (PBC), insulin resistance, amyloidosis, Cystic Fibrosis, Cholestasis, and Amyotrophic Lateral Sclerosis.
Taurodeoxycholic acid sodium hydrate (TUDCA) prevents apoptosis by blocking a calcium-mediated apoptotic pathway as well as caspase-12 activation. Taurodeoxycholic acid sodium hydrate is investigated for use in several conditions such as Primary Biliary Cirrhosis (PBC), insulin resistance, amyloidosis, Cystic Fibrosis, Cholestasis, and Amyotrophic Lateral Sclerosis. TUDCA abolished TG-induced markers of ER stress; reduced calcium efflux, induction of Bip/GRP78, and caspase-12 activation; and subsequently inhibited activation of effector caspases and apoptosis. Mitochondria play a secondary role in ER-mediated apoptosis and that TUDCA prevents apoptosis by blocking a calcium-mediated apoptotic pathway as well as caspase-12 activation[3]. Treatment with tauroursodeoxycholic acid (TUDCA), a hydrophilic bile acid, prevented neuropathology and associated behavioral deficits in the 3-nitropropionic acid rat model of HD (Huntington's disease). Systemically administered TUDCA led to a significant reduction in striatal neuropathology of the R6/2 transgenic HD mouse. R6/2 mice began receiving TUDCA at 6 weeks of age and exhibited reduced striatal atrophy, decreased striatal apoptosis, as well as fewer and smaller size ubiquitinated neuronal intranuclear huntingtin inclusions. Moreover, locomotor and sensorimotor deficits were significantly improved in the TUDCA-treated mice[4]. TUDCA reduces the damaging effects of TDCA (taurodeoxycholic acid) on fundus gastric mucosa; TUDCA may play an important role in the treatment of gastritis associated with bile reflux[5].
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