Role of Heat Shock Protein in Intestinal Ischemia and Reperfusion Injury

肠缺血再灌注(I/R)损伤。全身高温可诱导多个器官合成热休克蛋白(HSP)。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HSP70在小内含子中的表达。本实验研究了70 kDa热休克蛋白(HSP70)对体温过高小鼠小肠黏膜的影响，并通过磁共振波谱技术检测I/R过程中小肠能量代谢，评价了预先诱导的HSP70的细胞保护作用。磁共振波谱被用来作为能量代谢变化的标志。用Western印迹和免疫组织化学方法检测HSP70的表达。热休克蛋白70在加温后6~8h在小肠中的表达明显增加。为探讨热休克蛋白70(HSP70)的诱导对大鼠小肠I/R能量代谢的影响，将大鼠随机分为两组，分别给予或不给予全身热疗。夹闭肠系膜上动脉60min后再灌流，造成肠缺血。大鼠缺血前加温对缺血/再灌注损伤有明显的抵抗作用。非治疗组大鼠缺血时β-ATP值降低(37.1±15.5%)，再灌流时恢复，但仅为缺血前的55.0±10.0%。β-ATP值为缺血前的58.0±13.0%，再灌流时为缺血前的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.