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热暴露会引起不耐热的组织应激,但不会引起耐热的小鼠产生组织应激。

Heat exposure induces tissue stress in heat-intolerant, but not heat-tolerant, mice.

机构信息

Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.

出版信息

Stress. 2013 Mar;16(2):244-53. doi: 10.3109/10253890.2012.696754. Epub 2012 Jun 25.

DOI:10.3109/10253890.2012.696754
PMID:22632404
Abstract

We investigated the association of systemic and local tissue stress responses with heat-tolerant (TOL) levels in mice. Thirty-eight mice were assigned into control and three heat exposure groups-TOL, moderately tolerant, and intolerant (INT), based on their overall thermal responses. Real-time core temperature, blood pressure, and heart rate (HR) were assessed during heat exposure (39.5 °C) under conscious condition. Tissue samples were collected 18-22 h following heat exposure. INT mice had significantly higher peak mean arterial pressure and HR than TOL mice during heat exposure. Plasma corticosterone levels were significantly higher in INT than in control mice. No significant changes in plasma cytokines or markers of oxidative status were observed. INT mice showed significant increases in HSP72 and HSP90 protein and mRNA levels in liver, heart, and gastrocnemius muscles compared to TOL and control mice. In contrast, INT mice had significantly lower heat shock factor 1 and glucocorticoid receptor protein and mRNA levels in these tissues than TOL and control mice. These results indicate that acute heat exposure induces stress responses in various tissues of INT mice, but not TOL mice. Upregulation of stress proteins by acute heat exposure involves both transcriptional and translational pathways.

摘要

我们研究了全身性和局部组织应激反应与耐热(TOL)水平在小鼠中的关联。根据整体热反应,38 只小鼠被分为对照组和三个热暴露组——TOL、中度耐受和不耐受(INT)。在清醒状态下,在热暴露(39.5°C)期间评估实时核心温度、血压和心率(HR)。热暴露后 18-22 小时采集组织样本。与 TOL 小鼠相比,INT 小鼠在热暴露期间的平均动脉压和 HR 峰值显著升高。INT 小鼠的血浆皮质酮水平显著高于对照组。未观察到血浆细胞因子或氧化状态标志物有显著变化。与 TOL 和对照组小鼠相比,INT 小鼠的肝脏、心脏和比目鱼肌中的 HSP72 和 HSP90 蛋白和 mRNA 水平显著增加。相比之下,INT 小鼠的这些组织中的热休克因子 1 和糖皮质激素受体蛋白和 mRNA 水平显著低于 TOL 和对照组小鼠。这些结果表明,急性热暴露会引起 INT 小鼠的各种组织产生应激反应,但不会引起 TOL 小鼠产生应激反应。急性热暴露诱导应激蛋白的上调涉及转录和翻译途径。

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