Endoplasmic reticulum stress mediates lipopolysaccharide-induced apoptosis in rat hepatocyte / 法医学杂志
Journal of Forensic Medicine
; (6): 13-18, 2014.
Article
em Zh
| WPRIM
| ID: wpr-983872
Biblioteca responsável:
WPRO
ABSTRACT
OBJECTIVE@#To investigate the role of endoplasmic reticulum stress (ERS) in lipopolysaccharide (LPS)-induced hepatocyte apoptosis.@*METHODS@#Cells of the rat hepatocyte line BRL were cultured. The hepatocytes were treated with LPS, ERS inducer thapsigargin (TG), and ERS inhibitor 4-phenylbutyric acid (4-PBA), respectively or in their different combination. The cell viability was measured by MTT assay. The cyto-nuclear morphological changes of apoptosis cells were detected by the fluorescent dye Hoechst 33258. The apoptosis rate was assessed by flow cytometry with Annexin V-FITC/PI double-staining. Expressions of GRP78 as ERS marker protein, CHOP, caspase-12 and cleaved-caspase-3 as ERS related protein were detected by Western blotting.@*RESULTS@#LPS could cause a decrease in cell viability and an increase in apoptosis rate in a dose- and time-dependent manner. The expression of GRP78, CHOP, caspase-12 and cleaved-caspase-3 proteins were significantly increased with LPS treatment. TG led to a marked decrease in cell viability and an increase in apoptosis rate, which aggravated the hepatocyte injury induced by LPS; whereas 4-PBA alleviated LPS-induced apoptosis.@*CONCLUSION@#ERS mediates LPS-induced hepatocyte injuries, indicating that ERS may play a vital role in the pathogenesis of LPS-induced hepatocyte injuries.
Texto completo:
1
Base de dados:
WPRIM
Assunto principal:
Fenilbutiratos
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Sobrevivência Celular
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Lipopolissacarídeos
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Apoptose
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Hepatócitos
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Caspase 3
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Estresse do Retículo Endoplasmático
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Chaperona BiP do Retículo Endoplasmático
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Proteínas de Choque Térmico
Limite:
Animals
Idioma:
Zh
Revista:
Journal of Forensic Medicine
Ano de publicação:
2014
Tipo de documento:
Article