title: Inhibitory effect of somatostatin on prostaglandin E2 synthesis by primary neonatal rat glial cells.
abstract: Glial inflammation plays an integral role in the development of neurodegenerative disease. Although somatostatin is known to be a local anti-inflammatory factor in the periphery, evidence of a similar function in the brain is scarce. The aim of the present study was to investigate the effect of somatostatin on prostaglandin E(2) synthesis in primary neonatal rat glial cells. The data shows that high concentrations of somatostatin (10(-5)-10(-4)) significantly increased prostaglandin synthesis. By contrast, when used at physiologically relevant concentrations (10(-9)-10(-7) M), somatostatin and somatostatin receptor agonists decreased prostaglandin E(2) synthesis in non-stimulated glial cells as well as in lipopolysaccharide-induced prostaglandin synthesis. The inhibitory effect of somatostatin in lipopolysaccharide-treated cells could be mimicked by protein kinase A inhibitor and was prevented by forskolin. These observations suggest the presence of a novel neuro-immune feedback pathway through which somatostatin inhibits glial prostaglandin synthesis, and thus may prove to play a role in brain inflammation. This action of somatostatin may have a therapeutic potential in pathological conditions of the brain, where an inflammatory response is involved.
authors.affiliation: Department of Clinical Pharmacology, Ben-Gurion University of the Negev, P.O.B 653 Beer-Sheva, 84105, Israel.
authors.forename: Naama
authors.initials: N
authors.lastname: Dror
authors.forename: Liat
authors.initials: L
authors.lastname: Tveria
authors.forename: Inbal
authors.initials: I
authors.lastname: Meniv
authors.forename: Sarit
authors.initials: S
authors.lastname: Ben-Shmuel
authors.forename: Talia
authors.initials: T
authors.lastname: Filipovich
authors.forename: Sigal
authors.initials: S
authors.lastname: Fleisher-Berkovich
mesh_terms: D000577:Amides / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000166:cytology; D002478:Cells, Cultured; D005576:Colforsin / Q000494:pharmacology; D003470:Culture Media / Q000032:analysis / Q000737:chemistry; D016895:Culture Media, Serum-Free; D015232:Dinoprostone / Q000032:analysis / Q000096:biosynthesis*; D004305:Dose-Response Relationship, Drug; D004660:Encephalitis / Q000378:metabolism*; D006727:Hormone Antagonists / Q000378:metabolism* / Q000494:pharmacology; D007211:Indoles / Q000494:pharmacology; D007546:Isoquinolines / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism*; D009578:Nitrobenzenes / Q000494:pharmacology; D015282:Octreotide / Q000494:pharmacology; D011863:Radioimmunoassay; D051381:Rats; D017208:Rats, Wistar; D017481:Receptors, Somatostatin / Q000378:metabolism; D013004:Somatostatin / Q000031:analogs & derivatives / Q000378:metabolism* / Q000494:pharmacology; D013449:Sulfonamides / Q000494:pharmacology
chemical_list: D000577:Amides; C519495:BIM 23120; C519494:BIM 23926; D003470:Culture Media; D016895:Culture Media, Serum-Free; D006727:Hormone Antagonists; D007211:Indoles; D007546:Isoquinolines; C429627:L796778; C429628:L803087; D008070:Lipopolysaccharides; D009578:Nitrobenzenes; D017481:Receptors, Somatostatin; D013449:Sulfonamides; D005576:Colforsin; D013004:Somatostatin; D015232:Dinoprostone; C063509:N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; D015282:Octreotide