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Expression of heme oxygenase-1 in type II pneumocytes protects against heatstroke-induced lung damage.
Cell Stress and Chaperones ( IF 3.8 ) Pub Date : 2020-08-25 , DOI: 10.1007/s12192-020-01152-7
Chin-Kun Tseng , Tsung-Ta Liu , Tsung-Chieh Lin , Chia-Pi Cheng

Heatstroke (HS) is an acute clinical disease characterized by abnormal hyperthermia and multi-organ dysfunction. Heme oxygenase (HO)-1, also called heat shock protein (HSP)32, is induced by hyperthermia and also plays protective roles in many lung disease models. Based on this phenomenon, we investigated the protective role of endogenous HO-1 in heat-induced lung damage in rats. Male Sprague-Dawley (SD) rats were separated into three groups: (a) normothermic sham, (b) HS, and (c) SnPP (inhibitor of HO-1) pretreatment rats. In the HS group, rats were killed at various time points (1, 3, 6, and 12 h after heat exposure) in order to analyze messenger ribonucleic acid (mRNA) and protein levels. Lung sections were examined for tissue damage and localization of HO-1 using immunofluorescence double labeling. We found that HS induced lung pathology (congested and thickened lung septa). The level of HO-1 mRNA was increased at 1 h, and the protein level peaked at 6 h after heat exposure. Pretreatment with SnPP (tin-protoporphyrin IX, 30 mg/kg, intraperitoneal injection for 1 h before heat exposure) aggravated the lung damage. Furthermore, we demonstrated HO-1 expression in lung type II pneumocytes. Our results suggest that endogenous HO-1 is protective against HS-induced lung damage. Induction of HO-1 may be a potential therapeutic strategy for treating heat-related diseases.



中文翻译:

II型肺细胞中血红素加氧酶-1的表达可防止中暑引起的肺损伤。

中暑(HS)是一种以异常高热和多器官功能障碍为特征的急性临床疾病。血红素加氧酶 (HO)-1,也称为热休克蛋白 (HSP)32,由体温过高诱导,在许多肺部疾病模型中也发挥保护作用。基于这一现象,我们研究了内源性 HO-1 在大鼠热诱导肺损伤中的保护作用。雄性 Sprague-Dawley (SD) 大鼠分为三组:(a) 常温假手术,(b) HS,和 (c) SnPP(HO-1 抑制剂)预处理大鼠。在 HS 组中,在不同时间点(热暴露后 1、3、6 和 12 小时)处死大鼠以分析信使核糖核酸(mRNA)和蛋白质水平。使用免疫荧光双标记检查肺切片的组织损伤和 HO-1 的定位。我们发现 HS 诱发了肺部病变(肺间隔充血和增厚)。HO-1 mRNA 水平在 1 小时时增加,蛋白质水平在热暴露后 6 小时达到峰值。用 SnPP(锡原卟啉 IX,30 mg/kg,热暴露前腹腔注射 1 小时)预处理会加重肺损伤。此外,我们证明了 HO-1 在肺 II 型肺细胞中的表达。我们的结果表明内源性 HO-1 对 H2S 诱导的肺损伤具有保护作用。HO-1 的诱导可能是治疗热相关疾病的潜在治疗策略。此外,我们证明了 HO-1 在肺 II 型肺细胞中的表达。我们的结果表明内源性 HO-1 对 H2S 诱导的肺损伤具有保护作用。HO-1 的诱导可能是治疗热相关疾病的潜在治疗策略。此外,我们证明了 HO-1 在肺 II 型肺细胞中的表达。我们的结果表明内源性 HO-1 对 H2S 诱导的肺损伤具有保护作用。HO-1 的诱导可能是治疗热相关疾病的潜在治疗策略。

更新日期:2020-08-26
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