Ursodeoxycholic acid as a potential alternative therapeutic approach for neurodegenerative disorders: Effects on cell apoptosis, oxidative stress and inflammation in the brain
- PMID: 34632427
- PMCID: PMC7611783
- DOI: 10.1016/j.bbih.2021.100348
Ursodeoxycholic acid as a potential alternative therapeutic approach for neurodegenerative disorders: Effects on cell apoptosis, oxidative stress and inflammation in the brain
Abstract
Ursodeoxycholic acid (UDCA) is a bile acid component with anti-apoptotic, anti-oxidant and anti-inflammatory properties. It has been used in clinical medicine for liver diseases for centuries. In neurodegenerative diseases, increased cell apoptosis, oxidative stress and inflammation are frequently observed as well. Due to those beneficial effects of UDCA, recent studies have started to investigate the effects of UDCA in pre-clinical models of neurodegeneration. On this account, I review the data reported so far to investigate the role of UDCA in regulating apoptosis, oxidative stress and inflammation in pre-clinical models of neurodegeneration, as well as in homeostatic state. Evidence have shown that UDCA can reduce apoptosis, inhibit reactive oxygen species and tumor necrosis factor - α production in neurodegenerative models. In addition, UDCA is able to induce apoptosis of brain blastoma cells in homeostatic conditions. Overall, this review suggests the therapeutic potential of UDCA in neurodegenerative disorders, proposing UDCA as a potential alternative therapeutic approach for patients suffering from these diseases.
Keywords: Apoptosis; Inflammation; Neurodegeneration; Oxidative stress; Ursodeoxycholic acid.
Conflict of interest statement
Declarations of interest None.
References
-
- Abdelkader N.F., Safar M.M., Salem H.A. Ursodeoxycholic acid ameliorates apoptotic cascade in the rotenone model of Parkinson's disease: modulation of mitochondrial perturbations. Mol. Neurobiol. 2016;53:810–817. - PubMed
-
- Beuers U., Boyer J.L., Paumgartner G. Ursodeoxycholic acid in cholestasis: potential mechanisms of action and therapeutic applications. Hepatology. 1998;28:1449–1453. - PubMed
Grants and funding
LinkOut - more resources
Full Text Sources
