Mrs Jee-In Chung 1,2,3, Dr Eun Joo Baik 1,2,3
1 Department of Physiology, Ajou University School of Medicine, 2 Chronic Inflammatory Disease Research Center, Ajou University School of Medicine, 3 Brain Korea 21 for Medical Science, Ajou University School of Medicine
To prevent or treat neurodegenration such as epilepsy, stroke and Alzheimer’s disease, NSAID including COX-2 selective inhibitors is an emerging target. COX-2 is induced and a lot of prostaglandins (PGs) are released in the pathologic conditions; however the modulation of COX-2 activity in the nervous system was not clarified to be helpful to neurons or harmful. Using NSAID in the epidemiological studies, the incidence of Alzheimer’s disease is decreased, however clinical trial for Alzheimer’s disease with COX-2 selective inhibitor has been failed by little efficiency or cardiovascular accidents. It is due to little information about COX activity in the brain cells, which is composed with neurons and glial cells such as astocytes and microglial cells. In present study, COX activity in the brain cells was measured with the amount of PGs released from arachidonic acid(AA). Unlike other cells, AA-induced PGE2 release in neurons was not inhibited by COX inhibitors; however PGF2a from neurons was produced from COX-2. COX-independent PGE2 from neurons might not be related non-enzymatically from AA through isoprostane pathway. Neurons had PGES activities as much as those of the other cells. In conclusions, cortical neuron has different COX activity from other cells and produced PGF2a not PGE2 through COX. Understanding COX system in the nervous system is valuable to stand a strategy for treatment or prevention of neurodegenerative disease.
This study was supported by Chronic Inflammatory Disease Research Center (R13-2003-019-01005-0)
