Wen Ya-Ting, Liu Tsung-Ta, Lin Yuh-Feng, Chen Chun-Chi, Kung Woon-Man, Huang Chi-Chang, Lin Tien-Jen, Wang Yuan-Hung, Wei Li
1. Department of Neurosurgery, Taipei Medical University-Wan Fang Hospital, Taipei 11696, Taiwan.
2. Department of Biology and Anatomy, National Defense Medical Center, Taipei 114, Taiwan.
Int J Med Sci. 2015 Sep 4;12(9):737-41. doi: 10.7150/ijms.12517. eCollection 2015.
Exposure to high environmental temperature leading to increased core body temperature above 40°C and central nervous system abnormalities such as convulsions, delirium, or coma is defined as heat stroke. Studies in humans and animals indicate that the heat shock responses of the host contribute to multiple organ injury and death during heat stroke. Heme oxygenase-1 (HO-1)-a stress-responsive enzyme that catabolizes heme into iron, carbon monoxide, and biliverdin-has an important role in the neuroprotective mechanism against ischemic stroke. Here, we investigated the role of endogenous HO-1 in heat-induced brain damage in rats. RT-PCR results revealed that levels of HO-1 mRNA peaked at 0 h after heat exposure and immunoblot analysis revealed that the maximal protein expression occurred at 1 h post-heat exposure. Subsequently, we detected the HO-1 expression in the cortical brain cells and revealed the neuronal cell morphology. In conclusion, HO-1 is a potent protective molecule against heat-induced brain damage. Manipulation of HO-1 may provide a potential therapeutic approach for heat-related diseases.
暴露于高温环境导致核心体温升高至40°C以上，并出现惊厥、谵妄或昏迷等中枢神经系统异常，被定义为中暑。对人类和动物的研究表明，宿主的热休克反应会导致中暑期间多器官损伤和死亡。血红素加氧酶-1（HO-1）是一种应激反应酶，可将血红素分解为铁、一氧化碳和胆绿素，在对抗缺血性中风的神经保护机制中起重要作用。在此，我们研究了内源性HO-1在大鼠热诱导脑损伤中的作用。逆转录聚合酶链反应（RT-PCR）结果显示，热暴露后0小时HO-1 mRNA水平达到峰值，免疫印迹分析显示，热暴露后1小时蛋白质表达量最大。随后，我们检测了大脑皮层细胞中的HO-1表达，并揭示了神经元细胞形态。总之，HO-1是一种有效的抗热诱导脑损伤保护分子。调控HO-1可能为治疗与热相关的疾病提供一种潜在的治疗方法。
