ฉันรักการแปลProstaglandins and thromboxane A2 (TXA2), collectively termed prostanoids, are formed when arachidonic acid (AA), a 20-carbon unsaturated fatty acid, is released from the plasma membrane by phospholipases (PLAs) and metabolized by the sequential actions of prostaglandin G/H synthase, or cyclooxygenase (COX), and respective synthases.
There are four principal bioactive prostaglandins generated in vivo: prostaglandin (PG) E2 (PGE2), prostacyclin (PGI2), prostaglandin D2 (PGD2) and prostaglandin F2α (PGF2α).They are ubiquitously produced – usually each cell type generates one or two dominant products - and act as autacrine and paracrine lipid mediators to maintain local homeostasis in the body. During an inflammatory response, both the level and the profile of prostaglandin production changes dramatically. Prostaglandin production is generally very low in uninflamed tissues, but increases immediately in acute inflammation prior to the recruitment of leukocytes and the infiltration of immune cells.
Prostaglandin production (Figure 1) depends on the activity of prostaglandin G/H synthases, colloquially known as COXs, bifunctional enzymes that contain both cyclooxygenase and peroxidase activity and which exist as distinct isoforms referred to as COX-1 and COX-2 (2). COX-1, expressed constitutively in most cells, is the dominant source of prostanoids that subserve housekeeping functions, such as gastric epithelial cytoprotection and homeostasis (3). COX-2, induced by inflammatory stimuli, hormones and growth factors, is the more important source of prostanoid formation in inflammation and in proliferative diseases, such as cancer (3). However, both enzymes contribute to the generation of autoregulatory and homeostatic prostanoids, and both can contribute to prostanoid release during inflammation.
Figure 1
Figure 1
Biosynthetic pathway of prostanoids.