Arachidonic Acid Metabolites in Neurologic Disorders


Kursun O., KARATAŞ KURŞUN H., Bariskaner H., ÖZTÜRK Ş.

CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS, cilt.21, sa.2, ss.150-159, 2022 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 21 Sayı: 2
  • Basım Tarihi: 2022
  • Doi Numarası: 10.2174/1871527320666210512013648
  • Dergi Adı: CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Biotechnology Research Abstracts, EMBASE, MEDLINE
  • Sayfa Sayıları: ss.150-159
  • Anahtar Kelimeler: Arachidonic acid, COX, LOX, stroke, neurodegenerative diseases, PGs, CEREBRAL-BLOOD-FLOW, ALZHEIMERS-DISEASE, MOUSE MODEL, DOCOSAHEXAENOIC ACID, LIPID MEDIATORS, PROTEIN-KINASE, NEURODEGENERATIVE DISEASES, THERAPEUTIC STRATEGY, INTERNATIONAL UNION, PHOSPHOLIPASE A(2)
  • Hacettepe Üniversitesi Adresli: Evet

Özet

Background and Objective: Arachidonic acid (ARA) is essential for the fluidity, selective permeability, and flexibility of the cell membrane. It is an important factor for the function of all cells, particularly in the nervous system, immune system, and vascular endothelium. ARA is the second most common polyunsaturated fatty acid in the phospholipids of the nerve cell membrane after docosahexaenoic acid. ARA metabolites have many kinds of physiologic roles. The major action of ARA metabolites is the promotion of the acute inflammatory response, mediated by the production of pro-inflammatory mediators such as PGE2 and PGI2, followed by the formation of lipid mediators, which have pro-resolving effects. Another important action of ARA derivatives, especially COX, is the regulation of vascular reactivity through PGs and TXA2. There is significant involvement of ARA metabolites in neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and neuropsychiatric disorders. ARA derivatives also make an important contribution to acute stroke, global ischemia, subarachnoid hemorrhage, and anticoagulation-related hemorrhagic transformation.