In this study, we have compared the time-course effects of lipopolysaccharide (LPS) and interleukin-1beta on prostaglandin (PG) production by primary cultures of rat astrocytes. At variance with interleukin-1beta, LPS produced significant increases in PGE2 release after only 1 h of incubation, an effect unlikely to depend on new protein synthesis; the involvement of constitutive cyclooxygenase (COX-1) was therefore investigated. Experiments with acetylsalicylic acid showed that 80% of PGE2 production after 1 h of treatment with LPS is accounted for by COX-1; this figure decreases to about 30% after a 24-h treatment. The increase in PGE2 production occurring after a 24-h challenge with the endotoxin seems to involve the activation of phospholipase A2. In fact, LPS-stimulated PGE2 release was significantly reduced by a peptide from the primary sequence of lipocortin-1, peptide Ac2-26, which was previously shown to inhibit phospholipase A2 in several in vitro models.
Pistritto, G., Mancuso, C., Tringali, G., Perretti, M., Preziosi, P., Navarra, P. (1998). The relative contribution of constitutive and inducible cyclooxygenase activity to lipopolysaccharide-induced prostaglandin production by primary cultures of rat hypothalamic astrocytes. NEUROSCIENCE LETTERS, 246(1), 45-48.
The relative contribution of constitutive and inducible cyclooxygenase activity to lipopolysaccharide-induced prostaglandin production by primary cultures of rat hypothalamic astrocytes
PISTRITTO, GIUSEPPA;
1998-04-17
Abstract
In this study, we have compared the time-course effects of lipopolysaccharide (LPS) and interleukin-1beta on prostaglandin (PG) production by primary cultures of rat astrocytes. At variance with interleukin-1beta, LPS produced significant increases in PGE2 release after only 1 h of incubation, an effect unlikely to depend on new protein synthesis; the involvement of constitutive cyclooxygenase (COX-1) was therefore investigated. Experiments with acetylsalicylic acid showed that 80% of PGE2 production after 1 h of treatment with LPS is accounted for by COX-1; this figure decreases to about 30% after a 24-h treatment. The increase in PGE2 production occurring after a 24-h challenge with the endotoxin seems to involve the activation of phospholipase A2. In fact, LPS-stimulated PGE2 release was significantly reduced by a peptide from the primary sequence of lipocortin-1, peptide Ac2-26, which was previously shown to inhibit phospholipase A2 in several in vitro models.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.