摘要目的:探讨热暴露引起的氧化应激在跑台大鼠血压升高中的影响及抗氧化剂的干预作用。方法:于2021年6月，选择健康SD雄性大鼠24只，随机分为4组：常温饲养组、常温跑台组、高温跑台组和高温跑台补充维生素C组，每组6只。实验期为4周，每周进行6 d常温跑台或热暴露跑台，每天上、下午各30 min；高温跑台补充维生素C组大鼠每天补充维生素C剂量为10 mg/kg体质量。每周末测量血压。实验结束后，分离大鼠胸主动脉组织，收集血清，用ELISA法检测血管脂褐质（LF），用硝酸还原酶法检测血清一氧化氮（NO），用硫代巴比妥酸法检测血清丙二醛（MDA），用化学发光法检测血清谷胱甘肽过氧化物酶（GPx）、超氧化物歧化酶（SOD），用钼酸铵法检测血清过氧化氢酶（CAT），用铁还原/抗氧化能力法检测血清总抗氧化能力（T-AOC），采用Western blot法检测血管组织抗核转录相关因子2（Nrf2）含量。组内均数比较采用重复测量方差分析，组间均数比较采用单因素方差分析以及事后LSD- t检验。 结果:高温跑台组大鼠的收缩压和舒张压在7、14、21 d时与前一时间点比较均升高、28 d时有下降但高于初始水平（均 P<0.05），高温跑台组大鼠在各实验时间点收缩压、舒张压均高于常温跑台组（ P<0.001）；高温跑台组大鼠主动脉内膜光滑程度下降、纤维排列紊乱，中层厚度增加，显示有平滑肌细胞增殖情况；与常温跑台组比较，高温跑台组大鼠血清MDA和血管LF含量增高，血清SOD、CAT活力和T-AOC以及NO含量降低，血管组织中Nrf2表达量减少（ P<0.05）；与高温跑台组比较，高温跑台补充维生素C组大鼠7、14、21和28 d时收缩压和舒张压以及血清MDA和血管LF水平降低、CAT活力和T-AOC增高、血管组织中Nrf2表达量增加（ P<0.05），且血管内膜病理变化改善。 结论:热暴露对氧化应激有影响，其与热暴露大鼠血压升高密切相关；抗氧化增强剂维生素C对其有预防作用，可改善热暴露导致的大鼠血管内膜病理改变，Nrf2是一种血管保护调控因子。

abstractsObjective:To investigate the effect of oxidative stress caused by heat exposure on the blood pressure increase of treadmill rats and the intervention of antioxidants.Methods:In June 2021, Twenty-four healthy SD male rats were randomly divided into four groups: normal temperature feeding, normal temperature treadmill, high temperature treadmill and high temperature treadmill supplementation with vitamin C groups, 6 rats in each group. The rats run on the platform in normal temperature or heat exposure environment for 30 min in the morning and in the afternoon daily, 6 days per week. The daily vitamin C supplement dose of high temperature treadmill supplementation with vitamin C group was 10 mg/kg. BP recordings were done at the end of the week. The rat vascular lipofuscin (LF) was detected by ELISA, the rat serum nitric oxide (NO) was detected by nitrate reductase method, the serum malondialdehyde (MDA) was detected by thibabituric acid method, the serum glutathione peroxidase (GPx) and superoxide dismutase (SOD) were detected by chemiluminescence method, and the serum catalase (CAT) was detected by ammonium molybdate method. The total antioxidant capacity (T-AOC) of serum was measured by iron reduction/antioxidant capacity method, and the content of nuclear erythroid 2-related factor 2 (Nrf2) in vascular tissue was measured by Western blot. The intra-group mean was compared by repeated measurement analysis of variance, and the inter-group mean was compared by single-factor analysis of variance and post-event LSD- t test. Results:Compared with the previous time point, the systolic BP and diastolic BP of the high temperature treadmill group were significantly increased at 7, 14 and 21 d, and decreased at 28 d which were higher than the initial level ( P<0.05), and the systolic BP and diastolic BP values at each experimental time point were significantly higher than those of normal temperature treadmill group ( P<0.001). The changes of thickening of the artery wall, no smoothing of the endodermis and irregular arrangement of muscle cells in high temperature treadmill group were observed. Compared with the normal temperature treadmill group, the content of MDA in serum, and LF in vascular tissue were significantly increased, the activities of SOD, CAT, T-AOC, the content of NO in serum, and the expression of Nrf2 in vascular tissue were significantly decreased in high temperature treadmill group ( P<0.05). Compared with the high temperature treadmill group, the systolic BP and diastolic BP values at 7, 14, 21 and 28 d, the content of serum MDA and LF in vascular tissue were significantly decreased, the activities of CAT and T-AOC, and the expression of Nrf2 in vascular tissue significantly increased ( P<0.05), the histopathological changes of the artery wall improved in high temperature treadmill supplementation with vitamin C group. Conclusion:Heat exposure has effect on oxidative stress, which may be related to the increase of BP. Vitamin C as an anti-oxidative enhancer can prevent those negative effects, which could alleviate the pathological changes of vessel intima in heat-exposed rats. And the Nrf2 may be a regulated factor to vascular protection.