摘要
方法:从42只清洁级雄性SD大鼠中随机选取36只分为对照组(A组)、热应激组(B组)、有氧运动组(C组)与运动+热应激组(D组),剩余6只用于测定乳酸阈强度。各组实验后即刻测定血清IL-2、SOD、MDA等水平。结果:B、D组大鼠经热暴露后肛温均呈非常显著性升高,且出现典型的热应激症候。B组血清IL-2、SOD、SOD/MDA均显著低于A组,C组显著高于A组C组MDA显著低于A组;D组血清IL-2、SOD、SOD/MDA均显著低于A组(P<0.01)、B组(P<0.05)与C组(P<0.01),MDA显著高于A组(P<0.01)、B组(P<0.05)与C组(P<0.01)。结论:运动热应激可引起自由基生成增多,加重组织细胞膜的结构和功能损害,造成调节温度的信号通路发生中断,体温失衡;之后可能通过调节神经-内分泌-免疫系统机能,抑制IL-2的生成。IL-2可作为评定运动热应激过程中免疫机能的重要指标。
Objective： To evaluate influences of heat stress and/or exercise stress on immune function and antioxidant capacity.Methods： 36 of 42 healthy male SD rats were randomly selected and divided into control group（group A）,heat stress group（group B）,aerobic exercise group（group C）,and exercise and heat stress group（group D）,the remaining 6 for determination of lactate threshold strength.IL-2,SOD,MDA levels of each group were measured in serum obtained after experiment.Results： In group B,D,rectal temperature of rats raised significantly with typical symptoms of heat stress after heat exposure.In group B,levels of serum IL-2,SOD,SOD/MDA were significantly lower than that in group A,and group C was significantly higher than group A;In group C,MDA was significantly lower than group A;levels of IL-2,SOD,SOD/MDA were significantly lower in group D than that in group A（P0.01）,group B（P0.05） and group C（P0.01）,level of MDA was significantly higher than that in group A（P0.01）,group B（P0.05） and group C（P0.01）.Conclusion： Exercise heat stress may cause more free radicals,and increase damage of cell membrane structure and function of tissue,leading to interruption of the signaling pathways regulating the temperature,and imbalance of temperature.Possibly through regulation of nerve-endocrine-immune function and inhibition of IL-2 secretion.IL-2 can be used as an important indicator of immune function changes after body movement under heat stress
出处
《成都体育学院学报》
CSSCI
北大核心
2011年第4期86-90,共5页
Journal of Chengdu Sport University
