Effect of Minocycline on Activation of Glia and Nuclear Factor kappa B in an Animal Nerve Injury Model
The Korean Journal of Physiology and Pharmacology
; : 237-243, 2004.
Article
em En
| WPRIM
| ID: wpr-727918
Biblioteca responsável:
WPRO
ABSTRACT
Glial cells are activated in neuropathy and play a key role in hyperalgesia and allodynia. This study was performed to determine whether minocycline could attenuate heat hyperalgesia and mechanical allodynia, and how glial cell activation and nuclear factor kappa B (NF-kappaB) were regulated by minocycline in a model of chronic constriction of sciatic nerve (CCI). When minocycline (50 mg/kg, oral) was daily administered from 1 day before to 9 days after ligation, heat hyperalgesia and mechanical allodynia were attenuated. Furthermore, when minocycline treatment was initiated 1 or 3 days after ligation, attenuation of the hypersensitive behavior was still robust. However, the effect of attenuation was less when minocycline was started from day 5. In order to elucidate the mechanism of pain attenuation by minocycline, we examined the changes of glia and NF-kappaB, and found that attenuated hyperalgesia and allodynia by minocycline was accompanied by reduced microglial activation. Furthermore, the number of NF-kappaB immunoreactive cells increased after CCI treatment and this increase was attenuated by minocycline. We also observed translocation of NF-kappaB into the nuclei of activated glial cells. These results suggest that minocycline inhibits activation of glial cells and NF-kappaB, thereby attenuating the development of behavioral hypersensitivity to stimuli.
Palavras-chave
Texto completo:
1
Base de dados:
WPRIM
Assunto principal:
Nervo Isquiático
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Medula Espinal
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Neuroglia
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NF-kappa B
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Constrição
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Temperatura Alta
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Hiperalgesia
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Hipersensibilidade
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Ligadura
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Minociclina
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2004
Tipo de documento:
Article