Paper Information

Title: 

COX-1 ACTIVITY PRECEDES THE COX-2 INDUCTION IN Aβ INDUCED NEUROINFLAMMATION

Type: POSTER
Author(s): DARGAHI L.*,NASIRAEI MOGHADAM SH.,ABDI AZADEH,KHALAJ L.,AHMADIANI A.A.H.
 
 *NEUROSCIENCE RESEARCH CENTER, SHAHID BEHESHTI UNIVERSITY OF MEDICAL SCIENCES, TEHRAN, IRAN
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2009Volume 19
 
 
Abstract: 

Two different isoforms of cyclooxygenases, COX-1 and COX-2, are constitutively expressed under normal physiological conditions of CNS and accumulating data indicate that both isoforms may be involved in different pathological conditions. However, the distinct role of COX-1 and COX-2 and the probable interaction between them in neuroinflammatory conditions associated with Alzheimer’s disease is a conflicting issue. The aim of this study was elucidating the comparable role of each COX isoform in neuroinflammatory response induced by β-amyloid peptide (Aβ.) Using histological and biochemical methods, thirteen days after stereotaxic injection of Aβ into the rat prefrontal cortex, hippocampal neuroinflammation and neuronal injury confirmed by increased expression of TNF-α and COX-2, elevated levels of PGE2, astrogliosis, activation of caspase3 and neuronal cell loss. We used selective COX-1 or COX-2 inhibitors, SC-560 and NS-398 respectively, and retinoic acid, as an agent with proved anti inflammatory effects and potential ability to induce COX expression, for exploring the role of COX-1 and COX-2. Chronic treatment with either COX-1 or COX-2 selective inhibitor equally decreased the level of PGE2 to normal value and attenuated neuronal cell loss. Treatment with COX-1 selective inhibitor prevented the induction of COX-2. Chronic treatment with retinoic acid increased the expression of both COX isoforms and exacerbated the neural injury. The results indicate that the activity of both isoforms is detrimental in neuroinflammatory conditions associated with Aβ, but COX-1 activity is required for COX-2 induction and COX- 2 activity seems to be the main source of PGE2 increment.

 
Keyword(s): COX-1, COX-2, NEUROINFLAMMATION, β-AMYLOID PEPTIDE
 
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