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Effect of S‐adenosylmethionine versus tauroursodeoxycholic acid on bile acid‐induced apoptosis and cytolysis in rat hepatocytes
Author(s) -
Benz,
Angermüller,
KlötersPlachky,
Sauer,
Wolfgang Stremmel,
Stiehl
Publication year - 1998
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1998.00315.x
Subject(s) - tauroursodeoxycholic acid , bile acid , apoptosis , cytolysis , cholestasis , taurocholic acid , glutathione , ursodeoxycholic acid , chenodeoxycholic acid , medicine , alcoholic liver disease , chemistry , cirrhosis , pharmacology , biochemistry , endocrinology , biology , enzyme , cytotoxicity , in vitro , unfolded protein response
Background S‐adenosylmethionine (SAMe) increases survival in alcoholic liver cirrhosis and may have a beneficial effect in cholestatic liver disease. SAMe repletes glutathione stores and protects tissues from oxygen free radicals. The effect of SAMe on bile acid‐induced apoptosis is unknown. In the present study the possible hepatoprotective effect of SAMe was evaluated and compared with that of tauroursodeoxycholic acid (TUDCA). Methods Primary rat hepatocytes treated with glycochenodeoxycholic acid (GCDCA) were used as a model for cholestasis‐induced hepatocellular damage, which served to study the effects of SAMe and TUDCA on bile acid‐induced apoptosis and cytolysis. Results SAMe reduced bile acid‐induced apoptosis but did not prevent bile acid‐induced cytolysis. Compared with SAMe, TUDCA was more efficient in reducing apoptosis due to toxic bile acids. The combination of SAMe and TUDCA had additive effects in reducing apoptosis. Conclusion The reduction in bile acid‐induced apoptosis by SAMe may represent one of the factors responsible for its beneficial effects in the treatment of liver diseases.