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在普林格尔手法引起的肝脏热缺血损伤前,通过诱导热休克蛋白进行热休克预处理的保护作用。

Protective effect of heat shock pretreatment with heat shock protein induction before hepatic warm ischemic injury caused by Pringle's maneuver.

作者信息

Saad S, Kanai M, Awane M, Yamamoto Y, Morimoto T, Isselhard W, Minor T, Troidl H, Ozawa K, Yamaoka Y

机构信息

Second Department of Surgery, Kyoto University, Japan.

出版信息

Surgery. 1995 Sep;118(3):510-6. doi: 10.1016/s0039-6060(05)80367-8.

DOI:10.1016/s0039-6060(05)80367-8
PMID:7652687
Abstract

BACKGROUND

Induction of heat shock proteins is thought to have a > cytoprotective effect against environmental stress and to result in a better ischemic tolerance. The protective ability of heat exposure and heat shock protein 72 (HSP 72) induction before warm ischemia caused by Pringle's maneuver was evaluated in rats.

METHODS

Heat exposed rats (HS) were compared with control animals (C). The gene expression (messenger RNA) of HSP 72 and HSP 72 were detected by Northern and Western blot analyses. During 40 minutes of in situ reperfusion, liver energy metabolism and levels of standard liver enzymes were evaluated. The survival rate was determined after postoperative day 7.

RESULTS

After heat exposure and recovery, messenger RNA of HSP 72 and HSP 72 can be detected strongly in HS group but not in C group. During reperfusion HS group exhibited a significantly (p < 0.01) improved energy metabolism, and the release of liver enzymes was significantly (p < 0.001) reduced compared with C group. Seven-day survival rate was 100% in HS group but at 50% was significantly impaired (p < 0.05) in C group.

CONCLUSIONS

Heat exposure associated with HSP induction has a significant protective effect against warm ischemic liver injury, which results in a relevant improvement of survival rate.

摘要

背景

热休克蛋白的诱导被认为对环境应激具有细胞保护作用,并能产生更好的缺血耐受性。在大鼠中评估了热暴露和热休克蛋白72(HSP 72)诱导对普林格尔手法引起的温热缺血前的保护能力。

方法

将热暴露大鼠(HS)与对照动物(C)进行比较。通过Northern和Western印迹分析检测HSP 72的基因表达(信使RNA)和HSP 72。在原位再灌注40分钟期间,评估肝脏能量代谢和标准肝酶水平。在术后第7天测定存活率。

结果

热暴露并恢复后,HS组可强烈检测到HSP 72和HSP 72的信使RNA,而C组则未检测到。在再灌注期间,HS组的能量代谢显著改善(p < 0.01),与C组相比,肝酶释放显著减少(p < 0.001)。HS组的7天存活率为100%,而C组为50%,显著受损(p < 0.05)。

结论

与HSP诱导相关的热暴露对温热缺血性肝损伤具有显著的保护作用,这导致存活率的相关提高。

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