Renal abnormalities and an altered inflammatory response in mice lacking cyclooxygenase II.

摘要: Prostaglandins have wide-ranging effects in the body and are thought to be important mediators of inflammation. Cyclooxygenase (COX) plays a key regulatory role prostaglandin synthesis, occurs both constitutive (COX-1) inducible (COX-2) isoforms. COX-1 is provide cytoprotective effects, whereas COX-2 major isoform inflammatory cells. Reduction production by inhibition cyclooxygenases appears main mechanism action most non-steroidal anti-inflammatory drugs (NSAIDS). Here we present an animal model deficiency that was generated gene targeting. Defects null mice correlating with reduced viability included renal alterations, characteristic dysplasia (100% penetrance), cardiac fibrosis (50% penetrance). Female Cox-2-/- were infertile. failed alter responses several standard models, but striking mitigation endotoxin-induced hepatocellular cytotoxicity observed.