Endoplasmic reticulum stress collaborates with lipopolysaccharide to promote the inflammatory response in macrophages / 中华肝脏病杂志
Chinese Journal of Hepatology
; (12): 604-608, 2015.
Article
em Zh
| WPRIM
| ID: wpr-290392
Biblioteca responsável:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the protective mechanism of endoplasmic reticulum stress (ERS) inhibition against inflammation-induced acute liver injury using a mouse model.</p><p><b>METHODS</b>Marrow-derived stem cells were isolated from mouse femur and used to derive macrophages for analysis in experimental inflammation conditions, established by exposure to LPS and consequent activation of TLR4. Tunicamycin, an ERS chemical inducer, was applied to interfere the inflammation model condition.Affect on the inflammation-related factor MAPK was detected by western blot, and affects on gene expression of inflammatory factors were measured by real-time quantitative PCR. Affect on TNFa was also measured by ELISA.</p><p><b>RESULTS</b>Expression of TNFa, IL-6 and IL-1b was induced upon exposure to LPS, with the peak levels being reached at 4 hours of exposure (TNFa, 0.82+/-0.24; IL-1 b, 2.20+/-0.69; IL-6, 0.330+/-0.150). Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P<0.05; IL-1b, 16.063.40, t =7.93, P<0.05; IL-6, 31.1610.60, t=5.08, P<0.05). The tuniamycin treatment also enhanced the LPS-induced up-regulation of the protein expression of phospo-p38, phospho-JNK and phoshpo-ERK.</p><p><b>CONCLUSION</b>ERS collaborates with LPS to promote the TLR4-mediated inflammatory response of macrophages, and this collaboration may be a pathogenic mechanism underlying progressive development of acute liver injury.</p>
Texto completo:
1
Índice:
WPRIM
Assunto principal:
Regulação para Cima
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Lipopolissacarídeos
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Interleucina-6
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Modelos Animais de Doenças
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Receptor 4 Toll-Like
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Estresse do Retículo Endoplasmático
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Inflamação
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Fígado
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Macrófagos
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
Zh
Revista:
Chinese Journal of Hepatology
Ano de publicação:
2015
Tipo de documento:
Article