Academic Journal

Norepinephrine enhances the LPS-induced expression of COX-2 and secretion of PGE2 in primary rat microglia.

التفاصيل البيبلوغرافية
العنوان: Norepinephrine enhances the LPS-induced expression of COX-2 and secretion of PGE2 in primary rat microglia.
المؤلفون: Schlachetzki, Johannes C M, Fiebich, Bernd L, Haake, Elisabeth, de Oliveira, Antonio C P, Candelario-Jalil, Eduardo, HENEKA, Michael, Hüll, Michael
المصدر: Journal of Neuroinflammation, 7 (1), 2 (2010-01-11)
بيانات النشر: Springer Science and Business Media LLC
سنة النشر: 2010
المجموعة: University of Luxembourg: ORBilu - Open Repository and Bibliography
مصطلحات موضوعية: Adrenergic alpha-Agonists, Adrenergic beta-Antagonists, Imidazoles, Lipopolysaccharides, Propanolamines, RNA, Messenger, ICI 118551, CGP 20712A, Cyclooxygenase 2, Dinoprostone, Norepinephrine, Adrenergic alpha-Agonists/pharmacology, Adrenergic beta-Antagonists/pharmacology, Analysis of Variance, Animals, Newborn, Cells, Cultured, Cerebral Cortex/cytology, Cyclooxygenase 2/genetics, Cyclooxygenase 2/metabolism, Dinoprostone/metabolism, Dose-Response Relationship, Drug, Gene Expression Regulation, Enzymologic/drug effects, Imidazoles/pharmacology, Immunoenzyme Techniques/methods, Lipopolysaccharides/pharmacology
الوصف: peer reviewed ; [en] BACKGROUND: Recent studies suggest an important role for neurotransmitters as modulators of inflammation. Neuroinflammatory mediators such as cytokines and molecules of the arachidonic acid pathway are generated and released by microglia. The monoamine norepinephrine reduces the production of cytokines by activated microglia in vitro. However, little is known about the effects of norepinephrine on prostanoid synthesis. In the present study, we investigate the role of norepinephrine on cyclooxygenase- (COX-)2 expression/synthesis and prostaglandin (PG)E2 production in rat primary microglia. RESULTS: Interestingly, norepinephrine increased COX-2 mRNA, but not protein expression. Norepinephrine strongly enhanced COX-2 expression and PGE2 production induced by lipopolysaccharide (LPS). This effect is likely to be mediated by beta-adrenoreceptors, since beta-, but not alpha-adrenoreceptor agonists produced similar results. Furthermore, beta-adrenoreceptor antagonists blocked the enhancement of COX-2 levels induced by norepinephrine and beta-adrenoreceptor agonists. CONCLUSIONS: Considering that PGE2 displays different roles in neuroinflammatory and neurodegenerative disorders, norepinephrine may play an important function in the modulation of these processes in pathophysiological conditions.
نوع الوثيقة: article in journal/newspaper
اللغة: English
تدمد: 1742-2094
Relation: https://link.springer.com/content/pdf/10.1186/1742-2094-7-2.pdf; urn:issn:1742-2094; https://orbilu.uni.lu/handle/10993/61099; info:hdl:10993/61099; info:pmid:20064241; wos:000274830100001
DOI: 10.1186/1742-2094-7-2
الاتاحة: https://orbilu.uni.lu/handle/10993/61099
https://orbilu.uni.lu/bitstream/10993/61099/1/1742-2094-7-2.pdf
https://doi.org/10.1186/1742-2094-7-2
Rights: open access ; http://purl.org/coar/access_right/c_abf2 ; info:eu-repo/semantics/openAccess
رقم الانضمام: edsbas.CEA1F77D
قاعدة البيانات: BASE
الوصف
تدمد:17422094
DOI:10.1186/1742-2094-7-2