Editing TUDCA (tauroursodeoxycholic acid)
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== Effects on ALS == | == Effects on ALS == | ||
| − | TUDCA is a taurine-conjugated form of ursodiol and is commonly used for treatment of chronic cholestatic liver diseases and for gallstone. It possesses many additional ancillary features, including the inhibition of mitochondrial-associated apoptosis through different mechanisms. It has been shown that, in a cellular model of superoxide dismutase 1 neurodegeneration, glycine-conjugated UDCA inhibits nitrite production and prevents matrix metallopeptidase 9 activation | + | TUDCA is a taurine-conjugated form of ursodiol and is commonly used for treatment of chronic cholestatic liver diseases and for gallstone. It possesses many additional ancillary features, including the inhibition of mitochondrial-associated apoptosis through different mechanisms. It has been shown that, in a cellular model of superoxide dismutase 1 neurodegeneration, glycine-conjugated UDCA inhibits nitrite production and prevents matrix metallopeptidase 9 activation [1]. |
| − | At the end of the 54-week treatment period, patients in the TUDCA group had a mean ALSFRS-R score corresponding to that of the placebo group at week 36. This suggests that a 1-year TUDCA treatment may slow ALS deterioration by 18 weeks and leads us to suppose that a longer duration of treatment may produce an even more accentuated between-group divergence | + | At the end of the 54-week treatment period, patients in the TUDCA group had a mean ALSFRS-R score corresponding to that of the placebo group at week 36. This suggests that a 1-year TUDCA treatment may slow ALS deterioration by 18 weeks and leads us to suppose that a longer duration of treatment may produce an even more accentuated between-group divergence [1]. |
This study was designed to assess the effects of UDCA on oxidative injury and antioxidative systems in cultured rat hepatocytes. The viability of the hepatocytes dose-dependently decreased after hydrogen peroxide or cadmium administration. Pretreatment with UDCA significantly prevented this decrease in viability. The amounts of glutathione (GSH) and protein thiol increased significantly, but the activities of antioxidative enzymes such as superoxide dismutase, glutathione peroxidase and catalase were unchanged in UDCA-treated hepatocytes. The mRNA levels of gamma-glutamylcysteine synthetase and metallothionein (MT) were significantly higher in UDCA-treated hepatocytes than in controls. In conclusion, UDCA increased hepatocyte levels of GSH and thiol-containing proteins such as MT, thereby protecting hepatocytes against oxidative injury. {{#pmid:10491327|mitsuyoshi1999}} | This study was designed to assess the effects of UDCA on oxidative injury and antioxidative systems in cultured rat hepatocytes. The viability of the hepatocytes dose-dependently decreased after hydrogen peroxide or cadmium administration. Pretreatment with UDCA significantly prevented this decrease in viability. The amounts of glutathione (GSH) and protein thiol increased significantly, but the activities of antioxidative enzymes such as superoxide dismutase, glutathione peroxidase and catalase were unchanged in UDCA-treated hepatocytes. The mRNA levels of gamma-glutamylcysteine synthetase and metallothionein (MT) were significantly higher in UDCA-treated hepatocytes than in controls. In conclusion, UDCA increased hepatocyte levels of GSH and thiol-containing proteins such as MT, thereby protecting hepatocytes against oxidative injury. {{#pmid:10491327|mitsuyoshi1999}} | ||
