期刊
FEBS LETTERS
卷 590, 期 17, 页码 2813-2826出版社
WILEY-BLACKWELL
DOI: 10.1002/1873-3468.12313
关键词
Akt; mitogen-activated protein kinases; neuroinflammation; nuclear factor-kB; opioid receptor; PKCe
资金
- University of Ferrara
Increased production of proinflammatory cytokines has a prominent role in tolerance to opioids. The objectives of this study were to examine whether mu-opioid receptor affects proinflammatory signalling through the activation of NF-kB in microglia. The novelty of the described research is that a low dose of morphine, exerting its effects via the mu-opioid receptor, increases the DNA-binding activity of NF-kB via PKC epsilon, while a high dose of morphine triggers a nonopiate receptor response mediated by TLR4 and, interestingly, PKC epsilon signalling. The identification of morphine as a crucial upstream regulator of PKC epsilon-NF-kappa B signalling in microglia argues for a central role of these pathways in neuroinflammation development and progression. Therefore, the morphine-PKC epsilon-NF-kappa B pathway may provide novel targets to induce neuroprotective mechanisms, thereby reducing tolerance to opioids.
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