期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 182, 期 1-2, 页码 89-99出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2006.10.003
关键词
cytokines; inflammation; NF kappa B; oxidative stress; redox signaling
资金
- NCRR NIH HHS [P20 RR15592, P20 RR015592] Funding Source: Medline
- NIDA NIH HHS [P01 DA019398, P01 DA19398] Funding Source: Medline
- NINDS NIH HHS [R01 NS045601, NS45601, NS046267, R01 NS046267] Funding Source: Medline
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR015592] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS046267, R01NS045601] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [P01DA019398] Funding Source: NIH RePORTER
Activation of the oxidative burst is one of the earliest biochemical events in microglial activation, but it is not understood yet how free radicals participate in inflammatory signaling. To determine the role that specific reactive oxygen species play in microglial activation, the levels of SOD1 were manipulated in N9 murine microglia. Stable overexpression of SOD1 caused significant decreases in superoxide and nitric oxide production, with concurrent increases in hydrogen peroxide following LPS. However, LPS-induced activation of NF kappa B, and release of TNF alpha and IL-6 were significantly attenuated in SOD1 overexpressing cells, as was the ability of microglia to induce toxicity in cultured neurons. Conversely, acute inhibition of SOD1 with disulfiram was associated with increased nitric oxide and cytokine release, and increased neurotoxicity. Together, these data suggest that superoxide radicals in microglia, play important roles in directing redox-sensitive inflammatory signaling and initiating neurotoxic inflammation. (c) 2006 Elsevier B.V All rights reserved.
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