Previous heat shock facilitates the glutamine-induced expression of heat-shock protein 72 in septic liver.

OBJECTIVES: This study investigated the effects of glutamine administration on the expression of the heat-shock protein 72 (Hsp72) in the liver during sepsis. The role of heat-shock factor 1 (HSF-1) was analyzed for possible mechanisms to the phenomenon.

METHODS: Male Sprague-Dawley rats were subjected to sepsis by cecal ligation and puncture (CLP). Heat-shock treatment was applied to the rats' whole body using an electric heating pad 24 h before CLP. Glutamine or saline was administered 1 h after initiation of sepsis by tail vein injection. The Hsp72 and HSF-1 expressions were detected using western blot analysis, and Hsp72 mRNA expression was measured using reverse transcription-polymerase chain reaction.

RESULTS: The Hsp72 content noticeably increased in the livers of preheated rats supplied by glutamine 1 h after sepsis. However, no further synthesis of Hsp72 was found in septic livers or sham glutamine-treated livers. Hsp72, which was induced by preheating, decreased with time, whereas a large amount of Hsp72 could be detected by glutamine administration. Reverse transcription-polymerase chain reaction data indicated that Hsp72 mRNA could be detected only in the group treated with preheating and glutamine administration. The translocation of HSF-1 occurred significantly during sepsis in preheated and non-preheated rats. However, only the preheated group showed the phosphorylation in HSF-1. With the administration of glutamine, the nuclear accumulation of phosphorylated HSF-1 was observed to decline significantly 9 and 18 h after CLP when the Hsp72 mRNA became detectable.

CONCLUSIONS: These results demonstrated that Hsp72 could be induced by glutamine in septic liver only if the liver was preconditioned by heat-shock response. The selective facilitating effect might depend on the accumulation of intranuclear phosphorylated HSF-1 caused by previous heat-shock treatment.