Ontology highlight
ABSTRACT: Background
It has been proved that cyclo-oxygenase-2 (COX-2) is rapidly induced by inflammatory mediators. However, it is not known whether overexpression of COX-2 in the liver is sufficient to promote activation or secretion of inflammatory factors leading to hepatitis.Aim
To investigate the role forced expression of COX-2 in liver by using inducible COX-2 transgenic (TG) mice.Methods
TG mice that overexpress the human COX-2 gene in the liver using the liver-specific transthyretin promoter and non-TG littermates were derived and fed the normal diet for up to 12 months. Hepatic prostaglandin E(2) (PGE(2)) content was determined using enzyme immunoassay, nuclear factor kappaB (NF-kappaB) activation by electrophoretic mobility shift assays, apoptosis by terminal deoxy
SUBMITTER: Yu J
PROVIDER: S-EPMC1994375 | biostudies-literature | 2007 Jul
REPOSITORIES: biostudies-literature