Abstract
Here we compared the effects of cortistatin and somatostatin on the production of prostanoids from primary cultures of rat cortical microglia and astrocytes. We found that both cortistatin and somatostatin do not modify basal PGE(2) release from cultured astrocytes in 24-h experiments. Somatostatin further enhanced the increase in PGE(2) release induced by IL-1beta, whereas cortistatin inhibited such increase. Experiments on microglia showed that somatostatin has no effect on basal and IL-1beta-stimulated PGE(2) release, whereas cortistatin reduced baseline prostanoids production and abolished stimulation elicited by IL-1beta. The latter effect was associated to the inhibition of COX-2 gene over-expression induced by the cytokine.
MeSH terms
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Animals
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Animals, Newborn
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Anti-Inflammatory Agents / pharmacology
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Astrocytes / drug effects*
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Astrocytes / metabolism
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Cells, Cultured
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Cerebral Cortex / cytology
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Cerebral Cortex / drug effects*
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Cerebral Cortex / metabolism
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Cyclooxygenase 2 / biosynthesis
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Cyclooxygenase 2 / genetics
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Dinoprostone / biosynthesis
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Dinoprostone / metabolism
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Encephalitis / drug therapy
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Encephalitis / metabolism
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Encephalitis / physiopathology
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Gene Expression Regulation, Enzymologic / drug effects
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Gene Expression Regulation, Enzymologic / physiology
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Hormone Antagonists / pharmacology
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Hormones / pharmacology
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Inflammation Mediators / pharmacology
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Intercellular Signaling Peptides and Proteins
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Interleukin-1beta / agonists
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Interleukin-1beta / antagonists & inhibitors
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Microglia / drug effects*
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Microglia / metabolism
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Peptides / pharmacology*
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Prostaglandins / biosynthesis*
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Prostaglandins / metabolism
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Rats
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Rats, Wistar
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Somatostatin / pharmacology*
Substances
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Anti-Inflammatory Agents
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Hormone Antagonists
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Hormones
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Inflammation Mediators
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Intercellular Signaling Peptides and Proteins
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Interleukin-1beta
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Peptides
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Prostaglandins
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corticostatin
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Somatostatin
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Cyclooxygenase 2
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Dinoprostone