Role of Heat Shock Protein in Intestinal Ischemia and Reperfusion Injury

Research Project

Project/Area Number	10671209
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Digestive surgery
Research Institution	NAGOYA CITY UNIVERSITY
Principal Investigator	SATOH Atsushi NAGOYA CITY UNIV. MEDICAL SCHOOL. INSTRUCTOR, 医学部, 助手 (10275133)
Co-Investigator(Kenkyū-buntansha)	KUWABARA Yoshiyuki NAGOYA CITY UNIV. MEDICAL SCHOOL. ASSISTANT PROFESSOR., 医学部, 講師 (90225326)
Project Period (FY)	1998 – 1999
Project Status	Completed (Fiscal Year 1999)
Budget Amount *help	¥3,200,000 (Direct Cost: ¥3,200,000) Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000) Fiscal Year 1998: ¥2,700,000 (Direct Cost: ¥2,700,000)
Keywords	Small Intestine / Ischemia / Heat Shock Protein
Research Abstract	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.