cyanidanol 3/necrosis

Chlordecone (CD) pretreatment is well known to greatly potentiate CCl4 toxicity. Previous work has shown that suppression of hepatocellular regeneration permits an ordinarily limited liver injury to progress in an irreversible manner. Insufficient hepatocellular energy has been proposed as a

Pretreatment of rats with (+)cyanidanol--3 decreases the alterations in liver function tests (transaminase and bilirubin) as well as the accumulation of hepatic triglycerides induced by acute doses of galactosamine or carbon tetrachloride. This action was related to the dose of (+)cyanidanol-3

A number of immunomodulating agents of different origin have been shown to reduce liver injury of various etiologies. Immunostimulants like levamisole, BCG, a protein polysaccharide from myceria Coriolus vesicolor PS-K, a streptoccocal preparation OK-432 and immunomodulators like

On administration to rats at a subtoxic dose, the antibiotic nitrofurazone (NF) has been shown to increase hepatocyte DNA synthesis and liver weight in a dose-dependent manner, with no histological or biochemical evidence of cell damage or necrosis. Free radicals are implicated in NF metabolism, as

The antinecrotic potential of a new drug, 3-palmitoyl-(+)-catechin (PC), which is a derivative of (+)-cyanidanol-3, was studied in two different experimental models of necrosis of the liver in the rat: acute hepatitis induced by galactosamine and liver damage induced by a combination of chronic