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香叶基香叶基丙酮诱导热休克蛋白72减轻大鼠门静脉高压性胃黏膜乙醇诱导的损伤

Reduction of ethanol-induced injury in portal hypertensive gastric mucosa of rats by induction of heat shock protein 72 by geranylgeranylacetone.

作者信息

Kai Seiichiro, Ohta Masayuki, Tominaga Masayuki, Matsumoto Toshifumi, Bandoh Toshio, Kitano Seigo

机构信息

Department of Surgery I, Oita University Faculty of Medicine, Yufu, Oita, Japan.

出版信息

Wound Repair Regen. 2007 Nov-Dec;15(6):875-80. doi: 10.1111/j.1524-475X.2007.00302.x.

DOI:10.1111/j.1524-475X.2007.00302.x
PMID:18028136
Abstract

Portal hypertensive (PHT) gastropathy has an increased susceptibility to damage due to noxious factors. Heat shock protein (HSP) 72 has a protective effect against gastric mucosal injury and geranylgeranylacetone (GGA) is an inducer of HSP 72. However, it remains unclear how HSP 72 influences the PHT gastric mucosa. The aim of the present study was to investigate HSP 72 induction by GGA and the protective effect to gastric mucosa in PHT rats. PHT rats were produced by staged portal vein occlusion, and GGA 200 mg/kg was orally administered. Expression of HSP 72 protein in the gastric mucosa was evaluated by enzyme-linked immunosorbent assay, and gastric mucosal damage against 70% ethanol (10 mL/kg) following GGA or vehicle treatment was also estimated. Expression of mucosal HSP 72 after vehicle administration was significantly higher in the PHT rats compared with the sham-operated rats. After GGA treatment, portal pressure did not change but HSP 72 was significantly increased in the gastric mucosa of both groups. Ethanol-induced gastric mucosal damage was significantly decreased due to GGA treatment in the PHT rats, but not in the sham-operated rats. These findings suggest that HSP 72 expression is enhanced in PHT gastric mucosa and plays an important role in gastric mucosal protection. The induction of HSP 72 by GGA may therefore effectively prevent mucosal injury in the PHT stomach.

摘要

门脉高压性(PHT)胃病因有害因素而更易受损。热休克蛋白(HSP)72对胃黏膜损伤具有保护作用,而香叶基香叶基丙酮(GGA)是HSP 72的诱导剂。然而,HSP 72如何影响PHT胃黏膜仍不清楚。本研究的目的是探讨GGA对PHT大鼠HSP 72的诱导作用及其对胃黏膜的保护作用。通过分期门静脉结扎制备PHT大鼠,并口服给予200 mg/kg GGA。采用酶联免疫吸附测定法评估胃黏膜中HSP 72蛋白的表达,并评估GGA或赋形剂处理后胃黏膜对70%乙醇(10 mL/kg)的损伤情况。与假手术大鼠相比,PHT大鼠给予赋形剂后黏膜HSP 72的表达显著更高。GGA处理后,两组门静脉压力均未改变,但胃黏膜中HSP 72显著增加。GGA处理使PHT大鼠乙醇诱导的胃黏膜损伤显著减轻,但假手术大鼠未出现此现象。这些发现表明,HSP 72在PHT胃黏膜中的表达增强,并在胃黏膜保护中起重要作用。因此,GGA诱导HSP 72可能有效预防PHT胃的黏膜损伤。

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