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.
Prostaglandin Protection and Protection Mechanisms Against Lithocholic Acid Induced Hepatic Fibrosis in the Rabbit Tay, Jonathan S. (Kalamazoo College, 1987)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) ...
Kalamazoo College (2005-12-20)In an effort to properly protect the identity of each of its students and employees, Kalamazoo College has reviewed its use of social security numbers (SSNs) and has updated its practices to ensure, to the extent ...
Intitutional Review Board (2011)This policy's purpose is to protect human subjects of original research conducted either at Kalamazoo College or by an employee or student of Kalamazoo College. It is intended to assure that subjects of research are aware ...