Association between heat stress protein 70 induction and decreased pulmonary fibrosis in an animal model of acute lung injury
Association between heat stress protein 70 induction and decreased pulmonary fibrosis in an animal model of acute lung injury
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DOI：
10.1007/s00408-007-9018-x
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发表时间：
2007-09-01
期刊：
影响因子：
5
通讯作者：
Yoshioka, Hidekatsu
中科院分区：
文献类型：
--
作者：
Hagiwara, Satoshi;Iwasaka, Hideo;Yoshioka, Hidekatsu
高血压诱导的应激蛋白反应的激活允许细胞承受代谢损伤，否则将是致命的。这种现象被称为耐热性。热休克蛋白70（HSP 70）已被证明在这种高血压相关的细胞保护中发挥重要作用。HSP 70提供针对细胞和组织损伤的保护。我们的目的是确定热应激对脂多糖（LPS）致Wistar大鼠肺纤维化的组织病理学的影响。将大鼠随机分为3组。在对照组中，将大鼠加热至42 ℃ 15 min。在LPS组中，给予溶于0.9%NaCl溶液的LPS（10 mg/kg体重）。在WH（全身热疗）+LPS组中，将大鼠加热至42 ℃ 15 min，48 h后注射溶于0.9%NaCl溶液的LPS（10 mg/kg体重）。我们研究了肺组织病理学，并每天进行北方印迹分析。热疗被证明可以减少由LPS给药引起的组织损伤。肺组织HSP 70 mRNA在加热后3 h即开始升高。全身热疗后血清中HSP 70蛋白水平升高。然而，无论是热休克蛋白47 mRNA的表达，也没有I型或III型胶原mRNA的表达诱导全身热疗后的LPS管理。这些数据表明，热预处理与HSP 70蛋白合成的诱导，随后减弱在实验性肺纤维化的组织损伤。
The hyperthermia-induced activation of the stress protein response allows cells to withstand metabolic insults that would otherwise be lethal. This phenomenon is referred to as thermotolerance. Heat shock protein 70 (HSP70) has been shown to play an important role in this hyperthermia-related cell protection. HSP70 confers protection against cellular and tissue injury. Our objective was to determine the effect of heat stress on the histopathology of pulmonary fibrosis caused by the administration of lipopolysaccharide (LPS) in Wistar rats. The rats were randomly divided into three groups. In the control group, rats were heated to 42 degrees C for 15 min. In the LPS group, rats were given LPS in 0.9% NaCl solution (10 mg/kg body weight). In the WH (whole-body hyperthermia) +LPS group, rats were heated to 42 degrees C for 15 min, and 48 h later they were injected with LPS dissolved in a 0.9% NaCl solution (10 mg/kg body weight). We investigated lung histopathology and performed a Northern blot analysis daily. Hyperthermia was shown to reduce tissue injury caused by the administration of LPS. Pulmonary tissue HSP70 mRNA was found to be elevated at 3 h after heating. HSP70 protein levels in the serum increased after whole-body hyperthermia. However, neither the expression of HSP47 mRNA nor the expression of type I or type III collagen mRNA was induced by the administration of LPS after whole-body hyperthermia. These data indicate that thermal pretreatment is associated with the induction of HSP70 protein synthesis, which subsequently attenuates tissue damage in experimental lung fibrosis.