Tashiro Mitsuo, Ernst Stephen A, Edwards Julie, Williams John A
Department of Physiology, University of Michigan Medical School, Ann Arbor, 48109-0622, USA.
Digestion. 2002;65(2):118-26. doi: 10.1159/000057713.
Heat shock proteins (HSPs) which are induced by stress can provide protection against subsequent cellular damage. Whole body hyperthermia in rats leading to induction of HSP70 has been shown to protect against subsequent caerulein-induced acute pancreatitis. We studied the effect of hyperthermia on pancreatic HSP expression and found a significant increase in HSP70 (26.0-fold) and HPS27 (6.0-fold) but no change in HSP60, HSP90 or GRP78. Hyperthermia conferred significant protection against subsequent arginine-induced acute pancreatitis. More specifically, the degradation and disorganization of the actin cytoskeleton, an important early component of acute pancreatitis, was prevented. These results generalize previous work on caerulein-induced pancreatitis to another model of experimental pancreatitis, arginine-induced pancreatitis, and suggest that multiple HSPs may be involved in the cytoprotective effect in rat pancreas.
应激诱导产生的热休克蛋白(HSPs)可保护细胞免受后续损伤。研究表明,大鼠全身热疗可诱导HSP70产生,从而预防随后由蛙皮素诱导的急性胰腺炎。我们研究了热疗对胰腺HSP表达的影响,发现HSP70(26.0倍)和HPS27(6.0倍)显著增加,但HSP60、HSP90或GRP78无变化。热疗对随后由精氨酸诱导的急性胰腺炎具有显著的保护作用。更具体地说,可防止急性胰腺炎重要早期成分肌动蛋白细胞骨架的降解和紊乱。这些结果将先前关于蛙皮素诱导胰腺炎的研究推广至另一种实验性胰腺炎模型,即精氨酸诱导的胰腺炎,并表明多种HSPs可能参与大鼠胰腺的细胞保护作用。