Prostaglandin Protection And Protection Mechanism Against Lithocholic Acid Induced Hepatic Fibrosis in the Rabbit
Tay, Jonathan S.
MetadataShow full item record
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. Th i s study was under taken to determi ne if two prostaglandins, 16, 16-dimethyl prostaglandin E[;! (DMPGEe ), and 16, 16-dimethyl prostaglandin Fc~(J( (DMPGFe(J() also protect the liver from LCA induced hepatic fibrosis. The effectiveness of protection was evaluated according to serum bilirubin (BILl) and serum glutamic pyruvate transaminase (SGPT) levels; hepatic hydro xypro 1 i ne concentra t i on and content; and sta i nab Ie collagen in the liver. Rabbits were fed chow containing O.05X LCA. In rabbits pre and concomitantly treated with DMPGEI!'H reduced hydro xypro line concentra t ions in the livers and reduced BILl levels were conclusive evidence of protection. DMPGFe(J( had a favorable effect on BILl levels only. These data suggest that DMPGE~ 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 deter"mine if the prostaglandins caused precipitation of the toxin, and stomachs were examined for gastric lesions, to determine if the prostaglandins al tered the LCA absorption capacity of the stomach. Neither mechanism seemed to be likely. In a related study, rabbits were fed the O.05'l. LCA chow pr ior to treatment wi th DMPGE!!'! in order to determine if DMPGEe 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 DMPGE e 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.
Showing items related by title, author, creator and subject.
Malone, Frank Morris (1969)The title of the paper notwithstanding, the philosophy contained herein is essentially that of a free trader. When writing a paper such as this, however, it seems hard to make a dogmatic statement on the merits of free ...
The High Cost of Borrowing: An Intolerable Situation Created by Today's Inadequate Consumer Credit Protective Legislation Westerville, Mary Evelyn (1967)The intention of this thesis is to explore in more detail what has been previously said about "the high cost of borrowing" 'in consumer credit. Part 1 attempts to describe the diversified growth of the consumer credit ...