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热休克和替普瑞酮对乙醇诱导的培养兔胃黏膜细胞损伤的影响。

Effects of heat shock and teprenone on ethanol-induced damage to cultured rabbit gastric mucosal cells.

作者信息

Takahashi S, Yamazaki T, Okabe S

机构信息

Department of Applied Pharmacology, Kyoto Pharmaceutical University, Japan.

出版信息

J Physiol Pharmacol. 1996 Sep;47(3):433-41.

PMID:8877899
Abstract

We examined whether or not heat shock and teprenone (a gastric mucosal protective drug), through the induction of heat shock proteins (HSPs), protect cultured rabbit gastric mucosal cells from ethanol-induced damage. Cell viability was assessed by mitochondrial function and membrane permeability assays. Exposure of mucosal cells to 5% ethanol for 1h caused an about 50% reduction in viability. When the cells had been heated at 43 degrees C for 1 h, the cell damage caused by ethanol was significantly prevented. However, pretreatment with teprenone at 1-100 microM failed to prevent the ethanol-induced damage. Western blot analysis with an anti-HSP-72 antibody showed that HSP-72 was apparently induced by heat treatment, but not by teprenone. Both the cytoprotection and induction of HSP-72 on heat treatment were potently inhibited by cycloheximide and actinomycin D. These results demonstrate that, in rabbit gastric mucosal cells, the induction of HSPs is strongly associated with cytoprotection against ethanol-induced damage, but that teprenone has no effect on the cytoprotection or HSP induction.

摘要

我们研究了热休克和替普瑞酮(一种胃黏膜保护药物)是否通过诱导热休克蛋白(HSPs)来保护培养的兔胃黏膜细胞免受乙醇诱导的损伤。通过线粒体功能和膜通透性测定评估细胞活力。将黏膜细胞暴露于5%乙醇中1小时会导致活力降低约50%。当细胞在43℃加热1小时后,乙醇引起的细胞损伤得到显著预防。然而,用1 - 100微摩尔的替普瑞酮预处理未能预防乙醇诱导的损伤。用抗HSP - 72抗体进行的蛋白质印迹分析表明,HSP - 72明显由热处理诱导,而非替普瑞酮。环己酰亚胺和放线菌素D均能有效抑制热处理时的细胞保护作用以及HSP - 72的诱导。这些结果表明,在兔胃黏膜细胞中,HSPs的诱导与针对乙醇诱导损伤的细胞保护作用密切相关,但替普瑞酮对细胞保护作用或HSP诱导没有影响。

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