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Role of HMGB1 in propofol protection of rat intestinal epithelial cells injured by heat shock
Author(s) -
Tang Jing,
Deng Peng,
Jiang Yu,
Tang Youqing,
Chen Bin,
Su Lei,
Liu Zhifeng
Publication year - 2013
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10040
Subject(s) - hmgb1 , intracellular , heat shock protein , western blot , viability assay , heat shock , shock (circulatory) , microbiology and biotechnology , hsp70 , chemistry , inflammation , biology , pharmacology , cell , medicine , immunology , biochemistry , gene
Gut‐derived endotoxin and pathogenic bacteria may be important causative factors of morbidity and death during heat stroke. However, as the key component of intestinal mucosal barrier, the molecular mechanism of how intestinal epithelial cells are injured by heat shock is remains unclear. After rat intestinal epithelial cells (IEC‐6) had been exposed to heat shock, their viability was measured. Propofol, which plays an important role in anti‐inflammation and organ protection, was investigated to see how it affected viability under this stress. Changes of high mobility group box 1 (HMGB1) in IEC‐6 cells were measured with RT‐PCR and Western blot assay at transcription and translational levels, respectively. Ethyl pyruvate (EP), a specific inhibitor of HMGB1 that can inhibit the release of HMGB1 without affecting its intracellular synthesis, was also investigated. Heat shock significantly reduced the intracellular level of HMGB1, and propofol inhibit its reduction. Propofol protected the heat shock‐injured cells, at least partly through inhibiting the release of intracellular HMGB1 to reduce the direct or indirect cell damage caused by HMGB1. Pretreatment with high concentrations of EP also attenuated heat‐shock injury.