The role of TLR4-mediated MyD88-dependent pathway in neuroinflammation in hippocampal neurons of rats / 中国应用生理学杂志
Chinese Journal of Applied Physiology
;
(6): 42-46, 2013.
Artigo
em Chinês
| WPRIM
| ID: wpr-358683
ABSTRACT
<p><b>OBJECTIVE</b>To investigate weather there is a toll-like receptor 4 (TLR4)-mediated myeloid differentiation factor 88 (MyD88)-dependent pathway in hippocampal neurons of rats and the probable role of the pathway in neuroinflammation.</p><p><b>METHODS</b>To establish the proper model, primarily cultured hippocampal neurons were treated with lipopolysaccharides (LPS), or pretreated with TLR4 antibody then co-treated with LPS. The expression of mRNA of MyD88 and TNF-alpha receptor associated factor 6 (TRAF6) were tested by RT-qPCR. The content of MyD88 and TRAF6 were tested by Western blot. The nuclear translocation of nuclear factor-kappaB/P65 (NF-kappaB/p65) was tested by immunofluorescence. The content of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and nitric oxide (NO) were tested by ELISA.</p><p><b>RESULTS</b>LPS could increase MyD88 and TRAF6 mRNA, upregulate protein level of MyD88 and TRAF6 and increase the level of TNF-alpha, IL-1beta and NO in cell culture supernatant. LPS also could promote NF-kappa B/p65 translation to the nucleus. The pretreatment with TLR4 antibody reduced the translocation to nucleus for NF-kappaB/P65 and the contents of TNF-alpha, IL-1beta and NO in the culture supernatant.</p><p><b>CONCLUSION</b>There is a TLR4-mediated MyD88-dependent pathway in hippocampal neurons. The activation of this pathway can increase the level of TNF-alpha, IL-1beta and NO in cell culture supernatant. TLR4-mediated MyD88-dependent pathway in hippocampal neurons participate in neuroinflammation, that means neurons are not passive in inflammation.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Transdução de Sinais
/
Células Cultivadas
/
Fator de Necrose Tumoral alfa
/
Ratos Sprague-Dawley
/
Biologia Celular
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Fator 6 Associado a Receptor de TNF
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Fator de Transcrição RelA
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Receptor 4 Toll-Like
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Interleucina-1beta
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Fator 88 de Diferenciação Mieloide
Tipo de estudo:
Estudo prognóstico
Limite:
Animais
Idioma:
Chinês
Revista:
Chinese Journal of Applied Physiology
Ano de publicação:
2013
Tipo de documento:
Artigo
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