Learning Center

Tauroursodeoxycholic acid (TUDCA) reduces apoptosis and protects against neurological injury after acute hemorrhagic stroke in rats.

Reduction of brain injury underlies the wide-range neuroprotective effects of TUDCA after ICH. Thus, given its clinical safety, TUDCA may provide a potentially useful treatment in patients with hemorrhagic stroke and perhaps other acute brain injuries associated with cell death by apoptosis.


The Unexpected Uses of Urso- and Tauroursodeoxycholic Acid in the Treatment of Non-liver Diseases.

Several studies have demonstrated that TUDCA serves as an anti-apoptotic agent for a number of neurodegenerative diseases, including amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease, and Huntington's disease. In addition, TUDCA plays an important role in protecting against cell death in certain retinal disorders, such as retinitis pigmentosa.


Administration of tauroursodeoxycholic acid (TUDCA) reduces apoptosis following myocardial infarction in rat.

Results provide evidence for TUDCA as a viable treatment for reducing apoptosis in a model of myocardial infarction.


The chemical chaperones tauroursodeoxycholic and 4-phenylbutyric acid accelerate thyroid hormone activation and energy expenditure.

We now report that both TUDCA and 4-PBA are capable of activating the D2 pathway in a number of cell models and also when administered to mice.


Tauroursodeoxycholic Acid (TUDCA) Inhibits Respiratory Syncytial Virus Replication.

We found that RSV replication is significantly inhibited when infected cells were co-treated with TUDCA in a dose-dependent manner.


Tauroursodeoxycholic acid inhibits experimental colitis by preventing early intestinal epithelial cell death.

These data, together with the previously reported beneficial effect in colitis, suggest that TUDCA could be an add-on strategy to current immunosuppressive treatment of ulcerative colitis patients.

 


Tauroursodeoxycholic acid inhibits intestinal inflammation and barrier disruption in mice with non-alcoholic fatty liver disease.

TUDCA improved intestinal barrier function by increasing levels of tight junction molecules and the solid chemical barrier.


TUDCA prevents cholestasis and canalicular damage induced by ischemia-reperfusion injury in the rat, modulating PKCalpha-ezrin pathway.

TUDCA-treated livers showed increased bile flow and better preservation of microvilli and bile canalicular area at EM.


Tauroursodeoxycholic acid inhibits intestinal inflammation and barrier disruption in mice with non-alcoholic fatty liver disease.

TUDCA attenuates the progression of HFD-induced NAFLD in mice by ameliorating gut inflammation, improving intestinal barrier function, decreasing intestinal fat transport and modulating intestinal microbiota composition.


Stimulation of ATP secretion in the liver by therapeutic bile acids.

UDCA is rapidly conjugated to TUDCA in the liver, so the effects of both of these bile acids on isolated rat hepatocytes were examined. UDCA and TUDCA each induced isolated rat hepatocytes to release ATP, while three other bile acids had minimal or no effects


The Unexpected Uses of Urso- and Tauroursodeoxycholic Acid in the Treatment of Non-liver Diseases.

Obesity, stroke, acute myocardial infarction, spinal cord injury, and a long list of acute and chronic non-liver diseases associated with apoptosis are all potential therapeutic targets for T/UDCA.


Ursodeoxycholate modulates bile flow and bile salt pool independently from the cystic fibrosis transmembrane regulator (CFTR) in mice.

Our results in mice...When extrapolated to the human situation...might imply that UDCA treatment results both in CF and in non-CF individuals in increased choleresis, reduced bile salt synthesis, and a more hydrophilic bile salt pool.