双氧化锌(dl -天冬氨酸氢)诱导热休克蛋白70 (HSP70)可减轻大鼠缺血性小肠组织损伤。

C Töns, B Klosterhalfen, H M Klein, H M Rau, M Anurov, A Oettinger, V Schumpelick
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引用次数: 15

摘要

本研究的目的是确定Zn2+诱导HSP70是否能够保护大鼠小肠免受缺血。雄性Wistar大鼠24只(体重200 ~ 300 g),分为4组:(1)生理盐水处理24 h (n = 4);(2) Zn2+处理24h (n = 4);(3)盐水预处理24 h和缺血(n = 8);(4) Zn2+预处理24 h和缺血(n = 8)。Zn2+预处理采用50 mg/kg双锌(dl -天冬氨酸氢)= 10 mg/kg Zn2+腹腔注射。通过结扎肠系膜静脉和动脉以及结扎肠系膜静脉和动脉两端,在小肠某一特定节段产生缺血。分别于结扎前、结扎后2、4、6 h采集组织标本,进行组织学、免疫组织化学和Western blot检测。注射Zn2+ 24 h后,小肠组织表达HSP70水平升高。缺血组织损伤分级后的组织学显示,与盐水预处理对照组相比,Zn2+预处理和HSP70诱导后的组织坏死明显减少。综上所述,本研究证明Zn2+在体内诱导小肠HSP70,从而对小肠缺血具有保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Induction of heat shock protein 70 (HSP70) by zinc bis (DL-hydrogen aspartate) reduces ischemic small-bowel tissue damage in rats.

The aim of the study was to determine whether the induction of HSP70 by Zn2+ is able to protect the small bowel of rats against ischemia. Twenty-four male Wistar rats (weight 200-300 g) were divided into four groups: (1) saline treatment for 24 h (n = 4); (2) Zn2+ treatment for 24 h (n = 4); (3) Saline pretreatment for 24 h and ischemia (n = 8); (4) Zn2+ pretreatment for 24 h and ischemia (n = 8). Pretreatment with Zn2+ was carried out by intraperitoneal administration of 50 mg/kg zinc bis (DL-hydrogen aspartate) = 10 mg/kg Zn2+. Ischemia in a defined segment of the small bowel was produced by ligation of the mesenteric vein and artery and ligation of both ends of the segment. Tissue samples were collected before and 2, 4 and 6 h after ligation and investigated by histology, immunohistochemistry and Western blotting. Twenty-four h after i.p. Zn2+ injection, the small bowel expressed increased HSP70 tissue levels. Histology with subsequent grading of ischemic tissue injury showed significantly decreased tissue necrosis after Zn2+ pretreatment and HSP70 induction compared with saline pretreated controls. In conclusion, this study proves that Zn2+ is inducing HSP70 in the small bowel in vivo and hereby able to protect the small bowel against ischemia.

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