Jin M, Otaka M, Otani S, Okuyama A, Itoh S, Iwabuchi A, Sasahara H, Fujimori S, Itoh H, Tashima Y, Masamune O
First Department of Internal Medicine, Akita University School of Medicine, Japan.
J Gastroenterol. 1997 Feb;32(1):34-9. doi: 10.1007/BF01213294.
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 established. We examined the expression of HSPs in the small-intestinal mucosa after systemic hyperthermia, and evaluated the cytoprotective function of pre-induced HSPs on experimentally induced mucosal damage. HSP expression was investigated by Western blot and densitometric analysis before and after hyperthermia (42.5 degrees C; 20 min). Expression of a 72-kDa heat shock protein (HSP72) and a 73-kDa heat shock protein (HSP73), both of which are endogenous cytoprotectants in vitro significantly increased, peaking 6-9 h after hyperthermia, without any pathologic alterations, whereas the expression of a 60-kDa heat shock protein (HSP60) did not increase. To investigate the influence of pre-induction of HSPs on small-intestinal damage, rats received indomethacin (10 mg/kg; orally) with or without pre-treatment with hyperthermia. Small-intestinal damage caused by indomethacin was not influenced by pre-induction of HSP72 and HSP73. We demonstrated that systemic hyperthermia induced HSP72 and HSP73, although pre-induction of these proteins did not have a cytoprotective function in the small-intestinal damage caused by indomethacin.
全身热疗可诱导多个器官中热休克蛋白(HSPs)的合成。然而,小肠黏膜中HSPs的诱导机制及其功能尚未明确。我们检测了全身热疗后小肠黏膜中HSPs的表达,并评估了预先诱导产生的HSPs对实验性诱导的黏膜损伤的细胞保护功能。通过蛋白质印迹法和光密度分析对热疗(42.5℃;20分钟)前后的HSP表达进行了研究。一种72 kDa热休克蛋白(HSP72)和一种73 kDa热休克蛋白(HSP73)的表达在体外均为内源性细胞保护剂,二者表达均显著增加,在热疗后6 - 9小时达到峰值,且无任何病理改变,而一种60 kDa热休克蛋白(HSP60)的表达未增加。为研究预先诱导HSPs对小肠损伤的影响,大鼠口服吲哚美辛(10 mg/kg),部分大鼠在给药前进行热疗预处理。吲哚美辛所致的小肠损伤不受预先诱导HSP72和HSP73的影响。我们证明全身热疗可诱导HSP72和HSP73产生,尽管预先诱导这些蛋白对吲哚美辛所致的小肠损伤没有细胞保护作用。