Article

Kinins and neuroinflammation: dual effect on prostaglandin synthesis.

Department of Clinical Pharmacology, Ben-Gurion University of the Negev, P.O.B 653 Beer-Sheva 84105, Israel.
European Journal of Pharmacology (impact factor: 2.52). 10/2006; 546(1-3):197-200. DOI:10.1016/j.ejphar.2006.06.074 pp.197-200
Source: PubMed

ABSTRACT The role of kinins, well known as peripheral inflammatory mediators, in the modulation of brain inflammation is unclear. The present data show that bradykinin, a bradykinin B(2) receptor agonist, enhanced both basal and lipopolysaccharide-induced prostaglandin E(2) synthesis in rat neonatal glial cells in culture. By contrast, Lys-des-Arg(9)-bradykinin, which is a kinin breakdown product and a selective bradykinin B(1) receptor agonist, attenuated both basal and lipopolysaccharide-induced production of prostaglandin E(2) in glia. These results suggest a feedback regulatory mechanism of kinins on glial cells, in which prostaglandin synthesis is initially enhanced by bradykinin (B(2)) and eventually blocked by the effect of the kinin breakdown product, acting on bradykinin B(1) receptors.

0 0
 · 
0 Bookmarks
 · 
17 Views
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

basal
 
bradykinin
 
bradykinin B(1)
 
bradykinin B(2)
 
brain inflammation
 
feedback regulatory mechanism
 
kinin breakdown product
 
kinins
 
lipopolysaccharide-induced production
 
lipopolysaccharide-induced prostaglandin E(2)
 
Lys-des-Arg(9)-bradykinin
 
modulation
 
peripheral inflammatory mediators
 
prostaglandin E(2)
 
prostaglandin synthesis
 
rat neonatal glial cells
 
selective bradykinin B(1)
 

Avital Levant