Prostaglandin Protection and Protection Mechanisms Against Lithocholic Acid Induced Hepatic Fibrosis in the Rabbit
Tay, Jonathan S.
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Earlier studies have indicated that 16, 16-dimethyl prostaglandin E2 (DMPGE2) protects the rabbit liver from chenodeoxycholic acid induced hepatic fibrosis. Chenodeoxycholic acid is converted to lithocholic acid (LCA) by gut flora in the rabbit intestine. This study was undertaken to determine if two prostaglandins, DMPGE2, and 16, 16-dimethyl prostaglandin Fea (DMPGF2a) also protect the liver from LCA induced hepatic fibrosis. The effectiveness of protection was evaluated according to serum bilirubin (BILI) and serum glutamic , pyruvate transaminase (SGPT) levels; hepatic hydroxyproline concentration and content, and stainable collagen in the liver. Rabbits were fed chow containing 0.05'/ LCA. In rabbits pre- and concomitantly treated with DMPGE2, reduced hydroxyproline concentrations in the livers and reduced BILI levels were conclusive evidence of protection. DMPGF2a had a favorable effect on BILI levels only. These data suggest that DMPGES was protective against chenodoexycholic acid without directly influencing the conversion to LCA catalyzed by gut flora. To investigate the mechanism of this observed protection, bile taken from the gallbladders was examined for gall stones to determine if the prostaglandins caused precipitation of the toxin, and stomachs were examined for gastric lesions, to determine if the prostaglandins altered the LCA absorption capacity of the stomach. Neither mechanism seemed to be likely. In a related study, rabbits were fed the 0.05% LCA chow prior to treatment with DMPGE2 in order to determine if DMPGE2 had an effect on the reversal of the LCA induced hepatic fibrosis. Enhancement of reversal was not observed. Thus, potentiation of the regenerative capacity of the liver did not appear to be a likely mechanism of DMPGE2 protection. Other possible mechanisms that have not yet been investigated are the enhanced faecal excretion of the toxin, and the alteration of membrane fluidity resulting in the enhanced resistance to LCA by liver cells.
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Prostaglandin Protection And Protection Mechanism Against Lithocholic Acid Induced Hepatic Fibrosis in the Rabbit Tay, Jonathan S. (1987)Earlier studies have indicated that DMPGE~ protects the rabbit liver from chenodeoxycholic acid induced hepatic fibrosis. Chenodeoxycholic acid is converted to lithocholic acid (LCA) by gut flora in the rabbit intestine. ...
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