Endoplasmic reticulum stress mediates lipopolysaccharide-induced apoptosis in rat hepatocyte.
- Author:
Ying-Lei JI
;
Jun YAN
;
Yan-Sha WANG
;
Yi-Chang LIU
;
Zhen-Yong GU
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Caspase 3;
Cell Survival;
Endoplasmic Reticulum Chaperone BiP;
Endoplasmic Reticulum Stress;
Heat-Shock Proteins;
Hepatocytes;
Lipopolysaccharides;
Phenylbutyrates;
Rats
- From:
Journal of Forensic Medicine
2014;30(1):13-18
- CountryChina
- Language:Chinese
-
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.
