2013•Chinese HepatologyRequires access

The role of heat shock protein 27 in acute liver failure induced by pretreatment with lipopolysaccharide

Jianjia Zhang

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Abstract

Objective To investigate the role of heat shock protein 27(HSP27) in acute liver failure induced by pretreatment with lipopolysaccharide.Methods Male C57BL/6 mice were randomly divided into 5 groups:control group(with no treatment);liver injury group,which were injected intraperitonelly with D-Galn(700 mg/kg) and LPS(10μg/kg) dissolved in 1 mL sterile saline;LPS pretreatment group,which were injected with LPS(10μg/kg)24 hours before D-Galn/LPS treatment;HSP27 interference group,murine HSP27 was interfered by short hairpin RNA and mice were subjected to D-Galn/LPS with LPS pretreatment;Negative control group,which were also injected with vector virus and treated in the same way with HSP27 siRNA group.Serum ALT and AST levels,hepatic histological damages and mRNA levels of pro-inflammatory cytolines(TNF-αand IL-6) were measured.Results LPS pretreatment significantly reduced liver injury induced by D-Galn/LPS.The interference of HSP27 aggravated liver injury,which could be known from the higher levels of ALT and AST(P0.05),as well as the severer histological damage and more expression of TNF-αand IL-6(P0.05).Reducing the expression of HSP27 largely abrogated the protective effects induced by LPS pretreatment.Conclusion LPS pretreatment could protect against acute liver failure through HSP27 dependent pathways.

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Objective To investigate the role of heat shock protein 27(HSP27) in acute liver failure induced by pretreatment with lipopolysaccharide.Methods Male C57BL/6 mice were randomly divided into 5 groups:control group(with no treatment);liver injury group,which were injected intraperitonelly with D-Galn(700 mg/kg) and LPS(10μg/kg) dissolved in 1 mL sterile saline;LPS pretreatment group,which were injected with LPS(10μg/kg)24 hours before D-Galn/LPS treatment;HSP27 interference group,murine HSP27 was interfered by short hairpin RNA and mice were subjected to D-Galn/LPS with LPS pretreatment;Negative control group,which were also injected with vector virus and treated in the same way with HSP27 siRNA group.Serum ALT and AST levels,hepatic histological damages and mRNA levels of pro-inflammatory cytolines(TNF-αand IL-6) were measured.Results LPS pretreatment significantly reduced liver injury induced by D-Galn/LPS.The interference of HSP27 aggravated liver injury,which could be known from the higher levels of ALT and AST(P0.05),as well as the severer histological damage and more expression of TNF-αand IL-6(P0.05).Reducing the expression of HSP27 largely abrogated the protective effects induced by LPS pretreatment.Conclusion LPS pretreatment could protect against acute liver failure through HSP27 dependent pathways.

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Available abstract

Objective To investigate the role of heat shock protein 27(HSP27) in acute liver failure induced by pretreatment with lipopolysaccharide.Methods Male C57BL/6 mice were randomly divided into 5 groups:control group(with no treatment);liver injury group,which were injected intraperitonelly with D-Galn(700 mg/kg) and LPS(10μg/kg) dissolved in 1 mL sterile saline;LPS pretreatment group,which were injected with LPS(10μg/kg)24 hours before D-Galn/LPS treatment;HSP27 interference group,murine HSP27 was interfered by short hairpin RNA and mice were subjected to D-Galn/LPS with LPS pretreatment;Negative control group,which were also injected with vector virus and treated in the same way with HSP27 siRNA group.Serum ALT and AST levels,hepatic histological damages and mRNA levels of pro-inflammatory cytolines(TNF-αand IL-6) were measured.Results LPS pretreatment significantly reduced liver injury induced by D-Galn/LPS.The interference of HSP27 aggravated liver injury,which could be known from the higher levels of ALT and AST(P0.05),as well as the severer histological damage and more expression of TNF-αand IL-6(P0.05).Reducing the expression of HSP27 largely abrogated the protective effects induced by LPS pretreatment.Conclusion LPS pretreatment could protect against acute liver failure through HSP27 dependent pathways.

Key concepts: Hsp27, Lipopolysaccharide, Saline, Heat shock protein, Liver injury, Shock (circulatory), Tumor necrosis factor alpha, Liver failure

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