Role of HMGB1 in propofol protection of rat intestinal epithelial cells injured by heat shock
Role of HMGB1 in propofol protection of rat intestinal epithelial cells injured by heat shock
复制标题
HMGB1对异丙酚对热休克损伤大鼠肠上皮细胞的保护作用
DOI：
10.1002/cbin.10040
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发表时间：
2013-03-01
影响因子：
3.9
通讯作者：
Liu, Zhifeng
中科院分区：
文献类型：
--
作者：
Tang, Jing;Deng, Peng;Liu, Zhifeng
肠源性内毒素和致病菌可能是引起中暑发病和死亡的重要因素。然而，肠上皮细胞作为肠粘膜屏障的关键组成部分，其热休克损伤的分子机制尚不清楚。热休克后，测定大鼠肠上皮细胞（IEC-6）的生存能力。异丙酚在抗炎症和器官保护方面起着重要作用，研究人员研究了它在这种压力下如何影响生存能力。采用RT-PCR和Western blot法分别检测IEC-6细胞高迁移率组盒1 （HMGB1）在转录和翻译水平的变化。丙酮酸乙酯（EP）是HMGB1的特异性抑制剂，可以抑制HMGB1的释放而不影响其细胞内合成。热休克显著降低细胞内HMGB1水平，异丙酚抑制其降低。异丙酚对热休克损伤细胞的保护作用，至少部分是通过抑制细胞内HMGB1的释放来减轻HMGB1对细胞的直接或间接损伤。高浓度EP预处理也能减轻热休克损伤。
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.