Wang Faming, Lu Caiping, Lei Ying, Lei Tze-Huan
Centre for Molecular Biosciences and Non-Communicable Diseases, School of Safety Science and Engineering, Xi'an University of Science and Technology (XUST), Xi'an 710054, China.
Int J Mol Sci. 2025 May 26;26(11):5114. doi: 10.3390/ijms26115114.
Prolonged exposure to extreme humid heat can induce systemic inflammation, organ stress, and hormonal imbalance. While fluid replacement is commonly recommended, its mechanistic efficacy under humid heat stress remains unclear. This study investigated the impact of fluid intake on thermoregulation, inflammation, organ function, and stress signaling during 8 h of humid heat exposure (ambient temperature: 40 °C, relative humidity: 55%) in 32 healthy young adults (20 males and 12 females). Participants completed two randomized trials: limited fluid intake (LFI, 125 mL/h) and full fluid intake (FFI, 375 mL/h). Core temperature (), inflammatory cytokines (IL-6, IL-1β, IFN-γ, TNF-α), organ stress markers (ALT, BUN), oxidative stress indices (MDA, SOD), and cortisol were assessed pre- and post-exposure. FFI significantly reduced post-exposure (37.8 ± 0.3 °C vs. 38.1 ± 0.3 °C, = 0.046), mitigated cytokine elevations, and decreased BUN (blood urea nitrogen), ALT (alanine aminotransferase), and cortisol levels. Western blot analysis of PBMCs revealed that LFI activated NF-κB p65, JNK2, p38, and STAT3α phosphorylation, whereas FFI suppressed these responses. These findings demonstrate that adequate hydration attenuates heat-induced systemic and molecular stress responses. Our results highlight hydration as a key modulator of inflammatory signaling pathways during prolonged heat stress, offering insights into preventive strategies for populations vulnerable to climate-induced extreme heat events.
长时间暴露在极端湿热环境中会引发全身炎症、器官应激和激素失衡。虽然通常建议补充液体，但其在湿热应激下的作用机制尚不清楚。本研究调查了32名健康年轻成年人（20名男性和12名女性）在8小时湿热暴露（环境温度：40°C，相对湿度：55%）期间液体摄入对体温调节、炎症、器官功能和应激信号的影响。参与者完成了两项随机试验：限制液体摄入（LFI，125 mL/h）和充分液体摄入（FFI，375 mL/h）。在暴露前后评估核心体温（）、炎性细胞因子（IL-6、IL-1β、IFN-γ、TNF-α）、器官应激标志物（ALT、BUN）、氧化应激指标（MDA、SOD）和皮质醇。FFI显著降低了暴露后的核心体温（37.8±0.3°C对38.1±0.3°C，P = 0.046），减轻了细胞因子升高，并降低了BUN（血尿素氮）、ALT（丙氨酸转氨酶）和皮质醇水平。对PBMCs的蛋白质印迹分析显示，LFI激活了NF-κB p65、JNK2、p38和STAT3α磷酸化，而FFI抑制了这些反应。这些发现表明，充足的补水可减轻热诱导的全身和分子应激反应。我们的结果强调了补水是长时间热应激期间炎症信号通路的关键调节因子，为易受气候诱发的极端高温事件影响的人群提供了预防策略的见解。
