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Bile acid is the main component of bile, divided into primary bile acid (cholic acid, chenodeoxycholic acid) and secondary bile acid (deoxycholic acid, chitroic acid). UDCA derived from chenodeoxycholic acid is a small component (<5%) of the normal bile acid pool.
Most chronic cholestatic liver disease is caused by progressive loss or destruction of intrahepatic bile ducts. Bile duct epithelial lesions lead to bile acid transport disorders, increased serum bile acid concentration, the most common feature is the bile acid in the liver and blood accumulation with bile flow reduction.
Chronic cholestasis of liver injury mainly by intrahepatic deposition of high concentrations of hepatocytic toxic hydrophobic bile acids (such as lithocholic acid and its precursor chenodeoxycholic acid) mediated, they dissolve the cell membrane lipid caused by cell membrane damage, cell integrity damage, intracellular component leakage and hepatocyte hardening, can also lead to immune activation mediated liver injury.
UDCA treatment of cholestatic liver disease mechanism:
UDCA is a 7-beta isomer of chenodeoxycholic acid, which is efficiently absorbed in the liver and is primarily associated with glycine, which is secreted into the bile with the intestinal circulation. Under normal circumstances, taking UDCA will increase bile flow and secretion into the bile of bile acids, bile concentration increased by 50% with chenodeoxycholic acid and cholic acid. The same dose of UDCA and toxic bile acids (1% deoxycholic acid) were used to reverse the increase in serum total bilirubin and total bile acids and the decrease in cytochrome P450 content in hepatocytes.

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