Role of Heat Shock Protein in Intestinal Ischemia and Reperfusion Injury

肠缺血再灌注损伤。全身热疗诱导热休克蛋白（HSPs）在几个器官的合成。然而，热休克蛋白在小肠粘膜中的诱导机制和功能尚不清楚。我们检测了HSP 70在小肠中的表达。本实验研究了热休克蛋白70（70-kDa heat shock protein，HSP 70）对全身热疗后小肠黏膜的影响，并通过磁共振波谱（MRI）检测小肠缺血再灌注（I/R）过程中能量代谢的变化，评价了热休克蛋白70的细胞保护作用。磁共振波谱被用作能量代谢变化的标志。Western blot和免疫组化检测HSP 70表达。热疗后6-8小时小肠组织中HSP 70表达明显增加。为探讨热休克蛋白70（HSP 70）的诱导对大鼠小肠缺血再灌注（I/R）时能量代谢的影响，将大鼠随机分为两组，分别给予全身热疗和不给予全身热疗。通过夹闭上级肠系膜动脉60 min然后再灌注来诱导肠缺血。缺血前加热的大鼠赋予实质性的抵抗缺血/再灌注损伤。未治疗组大鼠脑缺血时β-ATP含量下降（为缺血前的37.1±15.5%），再灌注时恢复，但仅为缺血前的55.0±10.0%。而预处理组大鼠的β-ATP含量在缺血时仍为缺血前的58.0±13.0%，再灌注时达缺血前的88.0±16.4%。

Intestinal ischemia and reperfusion (I/R) injury. Systemic hyperthermia induces the synthesis of heat shock proteins (HSPs) in several organs. However, the mechanism of induction and the functions of HSPs in the small intestinal mucosa have not been made clear. We examined the expression of HSP70 in the small intes. We studied the effect of 70-kDa heat shock protein (HSP70) on small tinal mucosa after systemic hyperthermia, evaluated the cytoprotective function of pre-induced HSP70 by measurement energy metabolism of small intestine during I/R by using magnetic resonance spectroscopy. Magnetic resonance spectroscopy was employed as a marker of the changes in the energy metabolism. HSP70 expression was investigated by Western blot and immunohistochemistry. Expression of HSP70 in the small intestine was significantly increased at 6-8 hrs after the hyperthermia. To investigate the effect of induction of HSP70 on small intestinal energy metabolism during I/R, rats were randomized two groups, with or without pretreatment with systemic hyperthermia. Intestinal ischemia was induced by clamping the superior mesenteric artery for 60 min followed by reperfusion. Preischemia heating of the rat conferred substantial resistance to the ischemia / reperfusion injury. In the nontreatment rats, β-ATP decreased on ischemia (37.1±15.5% of the pre-ischemia value) and recovered on reperfusion, but reached only to 55.0±10.0% of the pre-ischemia value. However, β-ATP in the pretreatment rats continued on ischemia at 58.0±13.0% and on reperfusion reached to 88.0±16.4% of the pre-ischemia value.