Role of Heat Shock Protein in Intestinal Ischemia and Reperfusion Injury

热激蛋白在肠缺血再灌注损伤中的作用

• 批准号: 10671209
• 负责人: SATOH Atsushi
• 金额: $ 2.05万
• 依托单位: NAGOYA CITY UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1998
• 资助国家: 日本
• 起止时间: 1998 至 1999
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10671209/
• 关键词: Small Intestine; Ischemia; Heat Shock Protein

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.

肠缺血再灌注（I/R）损伤。全身热疗诱导多个器官合成热休克蛋白（HSPs）。然而，热休克蛋白在小肠黏膜中的诱导机制和功能尚不清楚。我们检测了HSP70在小肠中的表达。我们研究了70 kda热休克蛋白（HSP70）对全身热疗后小末代粘膜的影响，并采用磁共振波谱法测量I/R过程中小肠能量代谢，评价预诱导HSP70的细胞保护功能。采用磁共振波谱作为能量代谢变化的标志。Western blot和免疫组织化学检测HSP70的表达。热疗后6 ~ 8小时小肠中HSP70表达明显升高。为了研究诱导HSP70对I/R期间小肠能量代谢的影响，将大鼠随机分为两组，分别进行或不进行全身热疗预处理。采用夹紧肠系膜上动脉60 min后再灌注的方法诱导肠缺血。缺血前加热使大鼠对缺血再灌注损伤具有较强的抵抗能力。在未处理大鼠中，β-ATP在缺血时下降（为缺血前值的37.1±15.5%），再灌注时恢复，但仅为缺血前值的55.0±10.0%。而预处理大鼠的β-ATP在缺血时仍维持在58.0±13.0%，再灌注时达到缺血前的88.0±16.4%。

项目成果

Sato Atushi: "Intestinal energy metabolism during ischemia and reperfusiom"Journal of Surgioal Reserch. 82(2). 261-267 (1999)

Sato Atushi：“缺血和再灌注期间的肠道能量代谢”外科研究杂志。

Sato Atsushi: "Intestinal energy metabolism during ischemia and reperfusion"Journal of Surgical Research. 82(2). 261-267 (1999)

佐藤敦：“缺血和再灌注期间的肠道能量代谢”外科研究杂志。