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高峰气道压对大鼠肺组织热休克蛋白70表达的影响:一项初步研究。

Effects of high peak airway pressure on the expression of heat shock protein 70 in rat lungs: a preliminary study.

作者信息

Kira S, Mori M, Takatani J, Uchino T, Yasuda N, Miyakawa H, Noguchi T

机构信息

Department of Anesthesiology, Oita University Faculty of Medicine, Hasama-machi, Oita, Japan.

出版信息

Acta Anaesthesiol Scand. 2006 Apr;50(4):469-74. doi: 10.1111/j.1399-6576.2005.00942.x.

DOI:10.1111/j.1399-6576.2005.00942.x
PMID:16548859
Abstract

BACKGROUND

Heat shock protein 70 (HSP70) is induced by a wide variety of stresses in addition to hyperthermia. Recent studies have clarified that mechanical stretching and pressure overload can induce HSP70 in some tissues and cells. However, it remains unclear whether HSP70 is induced in stretch-subjected lungs, such as those under mechanical ventilation. This study was designed to investigate the effects of high peak airway pressure (PAP) ventilation on HSP70 expression in intact rat lungs.

METHODS

Male Sprague-Dawley rats were randomly allocated to one of three groups: non-ventilated (anesthesia alone) control group; PAP 15 cm H(2)O group (P15); and PAP 30 cm H(2)O group (P30). The rats in the PAP groups were subjected to pressure-controlled assisted ventilation at the appropriate PAP for 30 min. Rats were killed at 12, 24 and 48 h after ventilation or anesthesia alone, and the lungs were removed. The lung tissues were processed for immunohistochemical and Western blotting analyses of HSP70.

RESULTS

Following 30 min of pressure-controlled assisted ventilation, HSP70 expression in the P30 group was significantly up-regulated in bronchiolar cells and subepithelial tissues at 12 h, and this up-regulation continued throughout the observation period. In contrast, there were no significant differences between the control and P15 groups, although the expression of HSP70 was higher in the P15 group than in the control group at all time points.

CONCLUSIONS

HSP70 was induced by high PAP ventilation, but its specific role and induction mechanism remain unclear. Therefore, further investigations should be encouraged.

摘要

背景

热休克蛋白70(HSP70)除了在高热时被诱导产生外,还可被多种应激因素诱导。最近的研究表明,机械拉伸和压力过载可在某些组织和细胞中诱导HSP70的产生。然而,在诸如机械通气状态下的受牵拉肺组织中,HSP70是否会被诱导产生仍不清楚。本研究旨在探讨高峰气道压(PAP)通气对完整大鼠肺组织中HSP70表达的影响。

方法

雄性Sprague-Dawley大鼠被随机分为三组:非通气(仅麻醉)对照组;PAP 15 cm H₂O组(P15);PAP 30 cm H₂O组(P30)。PAP组的大鼠在适当的PAP下进行压力控制辅助通气30分钟。在通气或仅麻醉后12、24和48小时处死大鼠,并取出肺组织。对肺组织进行HSP70的免疫组织化学和蛋白质印迹分析。

结果

在压力控制辅助通气30分钟后,P30组细支气管细胞和上皮下组织中的HSP70表达在12小时时显著上调,并且在整个观察期内这种上调持续存在。相比之下,对照组和P15组之间没有显著差异,尽管在所有时间点P15组中HSP70的表达均高于对照组。

结论

HSP70可由高PAP通气诱导产生,但其具体作用和诱导机制仍不清楚。因此,应鼓励进一步研究。

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