期刊
BRAIN RESEARCH
卷 1395, 期 -, 页码 12-20出版社
ELSEVIER
DOI: 10.1016/j.brainres.2011.04.019
关键词
Rifampicin; Microglia; NF-kappa B; MAPKs; Neuronal cell; Neuroprotection
资金
- Guangdong Provincial Department of Science and Technology [0400935505B33801003]
- Ph.D. Programs Foundation of Ministry of Education of China [20070558257]
Microglial activation plays an important role in the pathophysiology of neurodegenerative diseases, and suppression of microglial activation prevents the progression of neurodegeneration. Rifampicin, a bacteriocidal antibiotic, induces immunosuppression. We hypothesized that rifampicin might be neuroprotective by inhibiting the production of pro-inflammatory mediators, thereby suppressing microglial activation. In the present study, we examined the effects of rifampicin on the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators and their signaling pathways in BV2 microglia. We also assessed the neuroprotective effects of rifampicin using a co-culture of microglia and neurons. Our results showed that rifampicin inhibited the LPS-stimulated expression of inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-alpha, and interleukin-1 beta, as well as the production of nitric oxide and prostaglandin E-2. Moreover, rifampicin suppressed LPS-induced nuclear factor-kappa B activation by blocking the degradation of the inhibitor of the nuclear transcription factor NF-kappa B. Rifampicin inhibited the phosphorylation of mitogen activated protein kinases, although protein kinase B was not inhibited. Preincubation of microglia with rifampicin reduced neurotoxicity and improved neuron survival in a microglia-neuronal co-culture system. Taken together, these findings suggest that rifampicin, with its anti-inflammatory properties, might be a novel treatment for neurodegenerative diseases. (C) 2011 Elsevier B.V. All rights reserved.
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