Heat stress increases the core body temperature through the pathogenic process. The pathogenic process leads to the release of free radicals, such as superoxide production. Heat stress in the central nervous system (CNS) can cause neuronal damage and symptoms such as delirium, coma, and convulsion. TRPV1 (Transient Receptor Potential Vanilloid1) and TRPV4 genes are members of the TRPV family, including integral membrane proteins that act as calcium-permeable channels. These channels act as thermosensors and have essential roles in the cellular regulation of heat responses. The objective of this study is to examine the effect of general heat stress on the expression of TRPV1 and TRPV4 channels. Furthermore, oxidative markers were measured in the brain of the same heat-stressed mice. Our results show that heat stress leads to a significant upregulation of TRPV1 expression within 21–42 days, while TRPV4 expression decreased significantly in a time-dependent manner. Alterations in the oxidative markers were also observed in the heat-stressed mice.

热应激通过致病过程增加核心体温。致病过程导致自由基的释放，例如超氧化物的产生。中枢神经系统 (CNS) 的热应激可导致神经元损伤和谵妄、昏迷和抽搐等症状。TRPV1（瞬时受体电位 Vanilloid1）和 TRPV4 基因是 TRPV 家族的成员，包括充当钙渗透通道的完整膜蛋白。这些通道充当热传感器，并在热反应的细胞调节中发挥重要作用。本研究的目的是检查一般热应激对 TRPV1 和 TRPV4 通道表达的影响。此外，在同一热应激小鼠的大脑中测量了氧化标志物。我们的结果表明，热应激导致 TRPV1 表达在 21-42 天内显着上调，而 TRPV4 表达以时间依赖性方式显着下降。在热应激小鼠中也观察到氧化标志物的变化。