高温对大鼠热应激蛋白的影响

在模拟高温环境下,测定大鼠热应激蛋白70kd(HSP 70)的合成,HSP70mRNA基因表达及肛温、心率、细胞形态学改变。探讨高温对HSP70的影响及HSP70在热应激中的作用。结果显示:高温使机体心率、体温升高,引起细胞损伤。三者与HSP70基因表达负相关。提示HSP70水平可成为判断机体热应激能力     

高温对大鼠热应激蛋白的影响

为了探讨高温环境对热应激蛋白（ＨＳＰ７０）的影响及ＨＳＰ７０在热应激中的作用，在模拟高温条件下，测定了大鼠ＨＳＰ７０的合成、ＨＳＰ７０ｍＲＮＡ基因的表达及肛温、心率、淋巴细胞形态学的改变。结果发现：机体心率加快、体温升高并伴有细胞损伤。三者与ＨＳＰ７０基因的表达呈负相关。提示：ＨＳＰ７０水平可成为判断机体热应激能力的敏感、特异指标。     

磁场、噪声、高温复合作用对大鼠热应激蛋白-70表达的影响

目的研究磁场、噪声、高温三因素复合作用对机体热应激蛋白-70(HSP70)表达的影响。方法采用三因素二水平正交方法[L8(27)]实验设计,用免疫组化ABC法测定大鼠肝脏、脾脏和脑组织的HSP70表达量。结果磁场对大鼠肝脏、脾脏和脑组织HSP70表达有影响(P<0.01或<0.05);高温对肝脏和脾脏组织中HSP70表达有影响(P<0.05)。结论磁场是影响HSP70表达的主因素,高温有一定的作用,磁场、高温、噪声三因素之间的交互作用不明显。     

山区和平原地区体育专业新生冷热应激水平差异比较

热应激蛋白(heat stress proteins,HSPs)是生物体细胞在一系列应激因素作用下产生的具有高度保守性的细胞保护性蛋白质,其中对HSP70的研究较多。当机体细胞遭受高温、缺血、缺氧等各种理化以及生物因素刺激时,HSP70合成显著增加,参与体内受损蛋白的清除和降解,对损伤细胞发挥保护作用[1]。本实验观察了来自不同海拔地区的体育专业新生的血液淋巴细胞在热应激条件下,其HSP70的表达,为HSP70在运动人体科学领域的应用提供实验参考。1对象与方法1.1对象与分组根据我国行政区划,结合海拔高度、常年温度及气象特征[2]划分山区和平原,生源地…     

热应激蛋白70与热应激反应

热应激蛋白(HSP)是机体在各种有害刺激条件下产生的一组高度保守的蛋白质，其中HSP70是最保守、最重要的一种。HSP70在各方面的应用都取得不少的进展，在热应激状态下对机体的保护作用是HSP70的一个重要研究方向。     

热适应与热应激对大鼠肝细胞HSP70表达的影响

目的 :研究不同时段的热适应及再经受热应激时大鼠肝细胞HSP70的表达变化及临床意义。方法 :采用人工热气候室 ,建立热适应 (34℃± 1℃、相对湿度 6 0 % )和热应激 (4 1℃± 1℃、相对湿度 80 % )动物模型。SD大鼠 16 0只 ,分为对照组、热适应组、热适应后热应激组、单纯热应激组 ,每组又分为 2、7、14、2 8d四个时段。取肝组织作免疫组化SP法染色 ,应用图像分析系统分析组织HSP70含量的变化。结果 :在热适应的四个时段 ,肝细胞的HSP70表达强度呈如下趋势 :热适应后热应激组 >热适应组 >对照组 ;单纯热应激组 >对照组 (P <0 .0 1或 0 .0 5 ) ;适应时段对HSP70表达强度变化无明显影响 ;2d时热适应组和热适应后热应激组的HSP70阳性枯否氏细胞数显著高于对照组 (P <0 .0 5 ) ,单纯热应激组与对照组无差别。结论 :热应激与热适应都可作为独立因素使肝细胞中HSP70表达增强 ,热适应加热应激则使HSP70表达更进一步加强 ;短时热适应使枯否氏细胞HSP70阳性表达明显增加     

热休克蛋白70与内毒素耐受性

热休克蛋白（HSP）是细胞受应激原刺激后诱导产生的一组应激蛋白，其中HSP70与内毒素耐受性有较密切的关系。不仅热可以诱导HSP70的表达，其它许多因素如Zn2 、脂多糖（LPH）等均可诱导HSP70的表达。HSP70可以通过细胞因子途径、NO途径和NF－kB等途径来调节内毒素耐受性。     

热应激对大鼠轴索损伤的保护作用

目的观察轴索损伤后相应的神经元及少突胶质细胞热休克蛋白70(HSP70)表达的变化及热应激对其表达的影响,探讨HSP70的神经保护作用. 方法 57只雄性Wistar大鼠随机分为正常对照组(A组,3只)、单纯视神经牵拉伤组(B组,18只)、单纯热应激处理组(C组,18只)和热应激预处理牵拉伤组(D组,18只).对B组大鼠右侧视神经施予牵拉,对C组大鼠施予热应激处理,D组大鼠热应激预处理24 h后再对右侧视神经施予牵拉,B、C、D组分别在4,8,16 h、1,3,5 d各处死3只大鼠.光镜下观察视神经、视网膜神经节细胞(RGCs)、视神经少突胶质细胞(OLs)的形态学变化,免疫组化染色检测RGCs及OLs HSP70表达情况. 结果牵拉伤后视神经轴索、RGCs及OLs的形态发生明显的病理变化,热应激预处理再致伤后上述病理改变有显著改善.单纯牵拉伤和单纯热应激处理均可使RGCs及OLs HSP70的表达增加,而热应激预处理再致伤使HSP70的表达明显增强,高峰表达时间提前,维持时间延长. 结论神经元及胶质细胞共同参与了轴索损伤后的病理过程.热应激能使HSP70表达增强、提前和延长,提高其神经保护作用.增强内源性神经保护作用是弥漫性轴索损伤(DAI)治疗的新途径.     

HSP70-hom基因多态性与高原反应易感性的关系

原核和真核生物在受到一系列理化因素如高温、毒物及某些重金属刺激后,可以启动热应激蛋白基因,诱导合成一组高度保守的蛋白质,称为热应激或热休克蛋白(heatstressproteins,HSPs)。HSP70是具有非常重要生物学意义的应激蛋白,作为分子伴侣,它可以促进蛋白质的合成、折叠、装配、运输,还参与变性蛋白质的消除等。HSPT0在生物进化过程中有高度保守性,其中HSP70-hom基因定位于6p21．3区主要组织相容性复合体(MHC)Ⅲ类分子内,存在于人类、大鼠和小鼠等物种体内,     

热休克蛋白与脑损伤的研究进展

热休克蛋白 (heatshockproteins ,HSPs)是指热应激时细胞新合成或合成增加的一类蛋白质 ,首次是从热应激果蝇幼虫的唾液腺等部位分离出来并命名。后来研究发现 ,除热应激外 ,多种损伤性因素可使组织细胞HSPs合成增加 ,它可保护机体在严酷的环境下得以生存。HSPs是一个大家族 ,现已发现的成员包括HSP1 1 0、HSP90家族、HSP70家族、HSP60、低分子量HSP、HSP1 0和泛素(ubiquitin)。正常生理情况下 ,中枢神经系统内并无HSPs的表达。近年来 ,国内外关于HSPs在脑损伤后的表达的研究十分活跃 ,已经发现缺血、创伤、氧化应激等均可导…     

热休克蛋白70对中暑大鼠急性肺损伤的保护作用及机制研究

目的 观察热休克蛋白70(HSP70)对急性肺损伤的保护作用.方法 64只SD大鼠按随机数字表法分为假加热正常对照组(Sham组)、中暑组(HS组)、中暑加谷氨酰胺处理组(HS+GLN组)和中暑加槲皮素处理组(HS+QU组),每组16只.Sham组大鼠置于温度23℃,湿度55％ ± 5％环境中,其余3组大鼠置于模拟热气候动物舱(舱内温度39℃,相对湿度65％)内.监测大鼠直肠温度、收缩压和脉率,比较各组大鼠热应激反应的差异.以收缩压从峰值开始下降作为中暑的开始,之后将大鼠移至常温复温.分别在中暑恢复期0h和6h处死大鼠,每个时间点8只,留取支气管肺泡灌洗液(BALF)后分离肺脏组织行组织学观察.采用酶联免疫法检测BALF中的IL-1β、TNF-α和IL-6浓度,以及肺组织匀浆中的HSP70浓度.结果 与HS组和HS+QU大鼠比较,HS+GLN组大鼠承受更多的热负荷后才发生HS(P＜0.001),起病后的中位生存时间明显延长(P＜0.001).与Sham组比较,HS组大鼠肺组织匀浆HSP70浓度呈时间依赖性升高(P＜0.001);HS+GLN组HSP70浓度在各个时点与HS组比较均明显升高(P＜0.001),而HS+QU组的HSP70表达则受到明显抑制时点与Sham组比较差异无统计学意义(P＞0.05),但明显低于HS组和HS+GLN组(P＜0.001).与HS组和HS+QU组比较,HS+GLN组大鼠BALF中的IL-1β、TNF-α和IL-6浓度明显降低(P＜0.001),病理结果显示其肺损伤更轻(P＜0.001),而HS+QU组则相反.结论 HSP70具有保护HS大鼠急性肺损伤的作用,其机制可能与增强大鼠热耐受能力和抑制HS大鼠肺部炎症相关.     

微波热疗诱导大鼠胰腺HSP70和HSP60的表达

 目的 研究微波热疗对大鼠胰腺HSP60和HSP70表达的影响.方法 将多功能治疗仪置于大鼠腹部进行辐射,使肛温升至40～41℃,维持30 min.分别于热疗后不同时段测定胰腺HSP60和HSP70含量.结果 与对照组比较,HSP70和HSP60均于微波热疗后升高(P<0.05).HSP70高峰出现在12 h(3.2倍),36 h下降至对照组2倍.HSP60高峰出现于12 h(2.1倍),36 h轻度下降(1.9倍).结论 微波热疗可同时诱导大鼠胰腺HSP70和HSP60表达.     

高温环境下急性力竭运动对大鼠心肌HSP70及血浆心钠素的影响

目的:探讨高温环境下急性力竭运动对大鼠心肌组织HSP70及血浆心钠素(ANP)的影响。方法:雄性SD大鼠48只,随机分为安静对照组(C)、运动后即刻组(E)、高温暴露1小时组(H)、高温运动后即刻组(HE)、运动后24小时恢复组(E’)和高温运动后24小时恢复组(HE’)6组,每组8只。E、HE、E’、HE’组均进行一次性力竭跑台运动。H组在周围环境温度33℃、相对湿度50%的环境中高温暴露1小时。C、E、HE、H组在力竭运动后即刻宰杀,HE’、E’组分别在高温及常温下运动后均在温度23℃、相对湿度50%的常温环境下恢复24小时后宰杀。测试大鼠心肌组织HSP70及血浆ANP、血清CK-MB水平。结果:(1)E组和E’组HSP70表达量较C组显著升高(P<0.05,P<0.01),HE’组显著高于H组及E’组(P<0.01)。H组显著高于C组(P<0.01)。(2)E组ANP和CK-MB水平显著高于C组(P<0.01),HE组显著高于H组(P<0.05);E’组和HE’组分别显著低于E组和HE组(P<0.01)。结论:(1)高温和运动均会诱导心肌HSP70高表达且24小时后表达最高,高温环境增强了力竭运动引起的HSP70的高表达,这可能会对高温及运动后造成的心肌损伤有一定的修复作用。(2)力竭运动即刻血浆心钠素升高,改善了心肌血液供应,同时也提示心肌有潜在受损的可能,但高温环境并未加强力竭运动所致的心钠素水平的增加。     

Opioid antagonism, perceived exertion and tolerance to exercise-thermal stress.

In an attempt to investigate the physiological responses to opioid receptor blockade during exercise in the heat, five male volunteers completed two bouts of stationary cycling at 70% VO2max in a hot (33 degrees C765% RH) environment. Exercise was conducted following the administration of either naloxone or saline (4 mg i.v.) five minutes prior to exercise. A second 4 mg dose was administered at 25 minutes of exercise. Performance time was 11% shorter (p = 0.06), and RPE response was significantly higher at test termination on naloxone. No drug effect was observed on rectal or mean skin temperature during exercise. Forearm blood flow (FBF) was higher on naloxone, while exercise heart rates were lower on the drug versus saline. No significant changes were observed in estimated mean arterial pressure or gross sweat responses to exercise. Plasma immunoreactive beta-endorphin was significantly elevated in the naloxone trial only. Thus, while opioids may play some hemodynamic role during exercise in the heat, it appears that opioid mediation of the perceived stress of exercise contributes more to an individual's thermal tolerance. Additionally, the results suggest that perceptual and hemodynamic/cardiovascular responses that may be mediated by these peptides are dissociable phenomena.     

Responses of distance runners and sprinters to exercise in a hot environment

The responses of highly trained distance runners and track sprinters and age-matched untrained men were compared during bicycle ergometry in a 40 degree temperature-controlled environmental chamber. There were no differences among groups in rectal temperature following the 90 min exercise bout. Distance runners had a lower heart rate than either sprinters or untrained subjects. There was no difference in heart rate between sprinters and untrained subjects. Distance runners and sprinters had a much greater sweat rate than untrained subjects and dissipated a greater proportion of their total heat load by evaporation of sweat. Sprinters, however, had a lower sweat rate than distance runners in the hot environment and could only maintain as low a skin temperature as distance runners for 75 min of the 90 min session. Both aerobic training and anaerobic training confer some degree of protection from heat injury during exercise in a hot environment. However, sprinters have a higher heart rate and cannot sustain a low skin temperature as long as distance runners. Sprinters lost their advantage over untrained subjects in skin temperature after 75 min of exercise in a hot environment and did not have a lower heart rate than untrained subjects. Distance runners had a significantly lower heart rate and maintained a lower skin temperature than untrained subjects for the entire 90 min exercise bout.     

Sexual variations in thermoregulation during heat stress

Four male and three female physically fit, but untrained subjects performed a treadmill walking task in neutral (25 degrees C), warm (32 degrees C) and hot (40 degrees C) environments. The treadmill grade for each subject was based on 50% VO2 max as determined in a neutral environment. Environmental exposures were 2 h in duration divided into 40 min of rest, work, and recovery. No distinct sexual differences in rectal and skin temperature responses were observed in the three environments. The male subjects had higher heart rates and greater evaporative weight losses during exercise in all environments. The female subjects experienced less severe increases in metabolic requirements during work in the warm and hot environments than the male subjects. The greater percentage of increase in heart rates relative to changes in the metabolic cost of work in the females suggested a greater cardiovascular component of thermal regulation in the female than in the male subjects. The results of this study suggest that physically fit females are capable of working in the heat about as well as males when work load is relative to individual maximal aerobic capacity.     

Effects of acclimation on cognitive performance in soldiers during exertional heat stress

This study investigates the effects of exertional heat stress and acclimation status on physiological and cognitive performance. Forty male soldiers performed an exertional heat stress test (EHST) either in a cool (20 degrees C, 16 degrees C wet bulb globe temperature), or in a hot environment (40 degrees C, 29 degrees C wet bulb globe temperature), unacclimatized, or after 10 days of passive or active acclimation. Mean skin and tympanic (Tty) temperatures and heart rates (HR) measured physiological strain. A cognitive test (the computerized Cambridge Neuropsychological Test Automated Batteries attention battery) is administered before and immediately after EHST. EHST in hot conditions induced physiological heat stress (increase in Tty and HR), which caused mild deficits in attention in U group (decreased number of correct responses, and prolonged movement time). Acclimated (passive and active) soldiers suffered no detrimental effects of exertional heat stress, despite almost the same degree of heat strain, measured by Tty and HR.     

American College of Sports Medicine position stand. Exertional heat illness during training and competition

Exertional heat illness can affect athletes during high-intensity or long-duration exercise and result in withdrawal from activity or collapse during or soon after activity. These maladies include exercise associated muscle cramping, heat exhaustion, or exertional heatstroke. While certain individuals are more prone to collapse from exhaustion in the heat (i.e., not acclimatized, using certain medications, dehydrated, or recently ill), exertional heatstroke (EHS) can affect seemingly healthy athletes even when the environment is relatively cool. EHS is defined as a rectal temperature greater than 40 degrees C accompanied by symptoms or signs of organ system failure, most frequently central nervous system dysfunction. Early recognition and rapid cooling can reduce both the morbidity and mortality associated with EHS. The clinical changes associated with EHS can be subtle and easy to miss if coaches, medical personnel, and athletes do not maintain a high level of awareness and monitor at-risk athletes closely. Fatigue and exhaustion during exercise occur more rapidly as heat stress increases and are the most common causes of withdrawal from activity in hot conditions. When athletes collapse from exhaustion in hot conditions, the term heat exhaustion is often applied. In some cases, rectal temperature is the only discernable difference between severe heat exhaustion and EHS in on-site evaluations. Heat exhaustion will generally resolve with symptomatic care and oral fluid support. Exercise associated muscle cramping can occur with exhaustive work in any temperature range, but appears to be more prevalent in hot and humid conditions. Muscle cramping usually responds to rest and replacement of fluid and salt (sodium). Prevention strategies are essential to reducing the incidence of EHS, heat exhaustion, and exercise associated muscle cramping.