Rifampicin inhibits microglial inflammation and improves neuron survival against inflammation
Rifampicin inhibits microglial inflammation and improves neuron survival against inflammation
复制标题
DOI:
10.1016/j.brainres.2011.04.019
复制
发表时间:
2011-06-13
期刊:
影响因子:
2.9
通讯作者:
Tao, Enxiang
中科院分区:
文献类型:
--
作者:
Bi, Wei;Zhu, Lihong;Tao, Enxiang
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.