16,16-dimethyl prostaglandin E2 delays collagen formation in nutritional injury in rat liver†

Abstract

Chronic nutritional injury was induced in rats by a high-fat, lipotrope-deficient diet. The hepatoprotective effect of 16,16-dimethyl prostaglandin E2 on the deposition of collagen and fat was assessed by histological evaluation and measurement of hydroxyproline. Dose-response studies established that optimal protection was achieved by the twice daily administration of 16,16-dimethyl prostaglandin E2 at 100 micrograms per kg (subcutaneous) or 250 micrograms per kg (oral). 16,16-Dimethyl prostaglandin E2 and a crystalline analog [(p-acetamidobenzamido)phenyl ester of 16,16-dimethyl prostaglandin E2 significantly delayed both the deposition of collagen and the increase in hepatic hydroxyproline content. There was an excellent correlation between the histological assessment of collagen and the biochemical measurement of hydroxyproline. These data provide a rationale for the evaluation of prostaglandins in the treatment of human liver disease.

A study of the ameliorating effects of carnitine on hepatic steatosis induced by total parenteral nutrition in rats

“…The remaining liver was fixed in 10% formalin and embedded in paraffin, and the sections were stained with hematoxylin and eosin (HE) and Sudan IV for histopathological examination. The severity of hepatic steatosis was evaluated semi-quantitatively according to the following grading system suggested by Ruwart et al [7] : -: absence of steatosis. +: mild steatosis with presence of lipid, mainly macrovesicular, in no more than 1/3 hepatocytes.…”

Administration of prostaglandin E1 analog reduces rat hepatic and ito cell collagen gene expression and collagen accumulation after bile duct ligation injury

“…Hepatic fibrosis was produced with a 13-wk diet deficient in choline. This fibrosis histologically shares features with human alcoholic liver disease and morbid obesity (36). The effectiveness of PGE in this model is pertinent because it etiologically differs markedly from the bile stasis model and the toxin or immunological models previously mentioned.…”

Pge1–Induced No Reduces Apoptosis by D–Galactosamine Through Attenuation of Nf–Kb and Nos–2 Expression in Rat Hepatocytes

“…3 PGE 1 exerts most of its effects by promoting membrane stabilization, 4 , hepatocyte proliferation, 5 vasodilation, 6 and inhibition of fibrogenesis. 7 The preadministration of PGE 1 also reduces liver injury through the enhancement of inducible NO synthase (NOS-2) expression in hepatocytes. 8 Nevertheless, the detailed molecular mechanism through which PGE 1 regulates NOS-2 expression is not completely understood.…”