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Sodium tauroursodeoxycholate (TUDC) shows therapeutic effect on cholestasis [1, 2]. In human erythrocytes, it inhibited 2’,7’-bis-(carboxypropyl)-5(6)-carboxyfluorescein (BCPCF) efflux induced by bile salts with an IC50 value of 560 μM [3].

Cholestasis is the syndrome resulted from the impairment of the formation of bile, a vital function [4].

cVA-of-CLF means the canalicular vacuolar accumulation of cholyllysylfluorescein [1]. cVA of CLF is a parameter to indicate overall biliary secretion [5]. Incubation with 17βEG dose-dependently decreased the cVA-of-CLF in cells. 17βEG at a concentration of 50 μM decreased cVA-of-CLF by 40%. The simultaneous incubation with TUDC and 17βEG improved the decreased cVA by 24%. The simultaneous incubation with SAMe and 17βEG improved the decreased cVA by 18%. The simultaneous incubation with TUDC, SAMe and 17βEG improved the decreased cVA by 28%. But the effect of TUDC + SAMe was not significantly greater than the effect of either protectant alone [1].

In rats, intrahepatic cholestasis was induced by the administration of phalloidin at an i.p. dose of 500 μg/kg for 7 days. In these treated rats, bile flow was decreased, and activities of glutamic pyruvic transaminase, leucine aminopeptidase, serum alkaline phosphatase, and concentrations of bile acid, phospholipid and cholesterol were increased. But these effects were significantly suppressed by tauroursodeoxycholate. In these rats, excretion rates of biliary cholesterol and phospholipid were significantly improved by tauroursodeoxycholate [2].

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