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Title	5-aminoimidazole-4-carboxamide-1-B-4-ribofuranoside inhibits proinflammatory response in glial cells: a possible role of AMP-activated protein kinase
Alternative Title	AICAR as an anti-inflammatory molecule
Author	Giri, Shailendra Nath, Narendra Smith, Brian Viollet, Benoit Singh Avtar K. Singh, Inderjit
Contributor(s)	Journal of Neuroscience (Publisher)
Date	2004-01-14
Affiliation/College	College of Graduate Studies College of Medicine
Department	Pathology and Laboratory Medicine Pediatrics
Subject.MeSH	Neuroglia Astrocytes Microglia Inflammation AMP-Activated Protein Kinases AICA ribonucleotide NF-kappa B Cytokines Macrophages, Peritoneal Cells, Cultured Rats, Sprague-Dawley Models, Animal Nitric Oxide Synthase Nitric Oxide Synthase Type II Transcription Factors Multienzyme Complexes Aminoimidazole Carboxamide Cell Nucleus Active Transport, Cell Nucleus Lipopolysaccharides Protein-Serine-Threonine Kinases
Subject.LCSH	Neuroglia Astrocytes Microglia Inflammation NF-kappa B (DNA-binding protein) CCAAT-Enhancer-Binding Proteins Cytokines Macrophages Cell culture Sprague Dawley rats Rats as laboratory animals Nitric-oxide synthase Transcription factors Cell nuclei Biological transport, Active Society for Neuroscience
Description	Article written by researchers from the Department of Pediatrics and Pathology and Laboratory Medicine, Medical University of South Carolina;Department of Genetic, Development, and Molecular Pathology, Institut Cochin, Institut National de la Sante et de la Recherche Medicale, Centre National de la Recherche Scientifique, Rene Descartes University;and Department of Pathology and Laboratory Medicine, Ralph H. Johnson Department of Veterans Affairs Medical Center. Published in The Journal of Neuroscience, January 14, 2004, volume 24, number 2, pages 479-487. Includes abstract, references, and diagrams.
Collection	MUSC Faculty Journal Articles
Contributing Institution	Waring Historical Library (MUSC)
Rights	Copyright 2004, Society for Neuroscience (SfN).
Language	English
Type	Text
Format	application/pdf
Media Type	Periodicals
Resource Identifier	fja_0037_2004
Abstract	AMP-activated protein kinase (AMPK) is tightly regulated by the cellular AMP:ATP ratio and plays a central role in the regulation of energy homeostasis and metabolic stress. A pharmacological activator of AMPK, 5-amino-4-imidazole carboxamide riboside (AICAR) inhibited lipopolysaccharide (LPS)-induced expression of proinflammatory cytokines (tumor necrosis factor , interleukin-1, and interleukin-6) and inducible nitric oxide synthase in primary rat astrocytes, microglia, and peritoneal macrophages. AICAR attenuates the LPS-induced activation of nuclear factor B via downregulation of IB kinase / activity. It also inhibits nuclear translocation of CCAAT/enhancer-binding protein (C/EBP) transcription factor by inhibiting the expression of C/EBP-in brain glial cells. The dominant negative form of AMPK2 (D157A) and its antisense documents a possible role of AMPK in the regulation of the cellular proinflammatory process. AICAR also inhibited the production of inflammatory mediators in serum and their expression in CNS of rats injected with a sublethal dose of LPS by intraperitoneal injection. These observations in cultured cells as well as in the animal model suggest that AICAR may be of therapeutic value in treating inflammatory diseases.

5-aminoimidazole-4-carboxamide-1-B-4-ribofuranoside inhibits proinflammatory response in glial cells: a possible role of AMP-activated protein kinase

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