Lin Xiaojing, Lin Cheng-Hsien, Zhao Tingbao, Zuo Dan, Ye Zhujun, Liu Lin, Lin Mao-Tsun
Department of Spinal Cord Injury and Repair, Trauma and Orthopedics, Institute of Chinese PLA, General Hospital of Jinan Military Region, Shandong, China.
Department of Leisure and Tourism Management, Southern Taiwan University of Science and Technology, Tainan, Taiwan, ROC.
Chem Biol Interact. 2017 Mar 1;265:47-54. doi: 10.1016/j.cbi.2017.01.006. Epub 2017 Jan 16.
Heat stroke is characterized by hyperthermia, systemic inflammation, and multiple organ failure including arterial hypotension. This definition can be fulfilled by a rat model of heat stroke used in the present study. Anesthetized animals were exposed to heat exposure (43 °C for 70 min) and then returned to room temperature (26 °C) for recovery. One hour before heat exposure, an intraperitoneal dose of quercetin (30 mg/kg) or vehicle (normal saline 1 ml/kg) was administered to the experimental groups of rats. Additional injection was administered immediately after the onset of heat stroke. Immediately after the onset of heat stroke. Vehicle-treated rats displayed (i) hyperthermia; (ii) suppressed left ventricular function; (iii) decreased contents of cardiac total antioxiant capacity (e.g., superoxide dismutase, glutathione peroxidase, catalase); (iv) increased contents of cardiac oxidative capacity malondialdehyde and thiobarbituric acid reactive substances; (v) increased cardiac levels of pro-inflammatory cytokines tumor necrosis factor-α and interleukin-6; and (vi) decreased cardiac levels of an anti-inflammatory cytokine interleukin 10. Histopathologic and survival observation provided supportive evidence for biochemical analyses. These heat stroke reactions all can be significantly attenuated by quercetin therapy. Our data suggest that quercetin therapy might improve outcomes of heat stroke in rats by attenuating excessive hyperthermia as well as myocardial injury. The protective effects of quercetin could be attributed to anti-lipid peroxidative, anti-oxidant, and anti-inflammatory properties.
中暑的特征为体温过高、全身炎症反应以及包括动脉低血压在内的多器官功能衰竭。本研究中使用的大鼠中暑模型符合这一定义。将麻醉后的动物置于高温环境（43℃，持续70分钟），然后放回室温（26℃）进行恢复。在高温暴露前1小时，给实验组大鼠腹腔注射槲皮素（30毫克/千克）或赋形剂（1毫升/千克生理盐水）。中暑发作后立即进行额外注射。中暑发作后，接受赋形剂治疗的大鼠表现出：（i）体温过高；（ii）左心室功能受抑制；（iii）心脏总抗氧化能力（如超氧化物歧化酶、谷胱甘肽过氧化物酶、过氧化氢酶）含量降低；（iv）心脏氧化能力丙二醛和硫代巴比妥酸反应性物质含量增加；（v）心脏促炎细胞因子肿瘤坏死因子-α和白细胞介素-6水平升高；以及（vi）心脏抗炎细胞因子白细胞介素10水平降低。组织病理学和存活观察为生化分析提供了支持性证据。这些中暑反应均可通过槲皮素治疗得到显著缓解。我们的数据表明，槲皮素治疗可能通过减轻过度体温过高以及心肌损伤来改善大鼠中暑的预后。槲皮素的保护作用可能归因于其抗脂质过氧化、抗氧化和抗炎特性。
