Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 223, Issue 1-2, Pages 77-83Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2010.04.006
Keywords
beta-adrenergic receptor; Pro-inflammatory cytokine; Microglia; Surgical trauma stress; MAPK
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Funding
- National Key Basic Research Program of China [2006CB504509, 2007CB512502]
- Shanghai Scientific and Technological Innovation program [09dZ1974100]
- National Natural Science Foundation [30970975]
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Immunological changes initiated by major operative injury may result in inflammatory responses in both peripheral and central nervous system, which may lead to organ dysfunction. Recent studies indicate that beta-adrenergic receptors (beta-ARs) may mediate production of pro-inflammatory cytokines in the brain. In the present study propranolol (beta-AR antagonist), but not prazosin (alpha 1-AR antagonist), antagonized surgical trauma induced pro-inflammatory cytokine production in microglia cells isolated from rats. beta-AR activation in the absence of pro-inflammatory stimuli increased IL-1 beta, TNF-alpha and IL-6 mRNA and protein expressions in the primary microglia cell culture. Isoproterenol (beta-AR agonist) treatment induced a time- and concentration-dependent increase of IL-1 beta in cells. Both ERK1/2 and P38 MAPK inhibitor, but not PKA and JNK1/2 inhibitor abrogated isoproterenol-induced IL-1 beta and IL-6 production in microglia cells. In conclusion, the results suggest that beta-ARs possess pro-inflammatory properties by modulating the functions of microglia cell. (C) 2010 Elsevier B.V. All rights reserved.
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