These authors contributed equally to this work.
Role of HMGB1 in propofol protection of rat intestinal epithelial cells injured by heat shock
Article first published online: 30 JAN 2013
© 2013 International Federation for Cell Biology
Cell Biology International
Volume 37, Issue 3, pages 262–266, March 2013
How to Cite
Tang, J., Deng, P., Jiang, Y., Tang, Y., Chen, B., Su, L. and Liu, Z. (2013), Role of HMGB1 in propofol protection of rat intestinal epithelial cells injured by heat shock. Cell Biology International, 37: 262–266. doi: 10.1002/cbin.10040
- Issue published online: 8 FEB 2013
- Article first published online: 30 JAN 2013
- Accepted manuscript online: 4 JAN 2013 04:39AM EST
- Manuscript Accepted: 23 DEC 2012
- Manuscript Received: 4 NOV 2012
- heat stress;
- intestinal epithelial cells;
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.