摘要
目的:探寻一次较大强度的力竭性耐力跑运动后心肌过氧化损伤的PKCδ/NOX途径。方法:86只成年雄性SD大鼠,随机分为安静对照组(C)、安慰剂运动组(PE)、抑制剂运动组(DE)。根据实验设计,C组又随机分为安慰剂安静对照组(PC)与抑制剂安静对照组(DC)。DC、DE组采用PKCδ特异性抑制剂Rottlerin干预,PC、PE组采用安慰剂干预;随后DE、PE进行一次较大强度的力竭性跑台运动。PE、DE组又各随机分为运动后24 h、36 h的2组。比较心肌损伤指标,即血液c Tn I、CK-MB水平及心肌细胞超微结构等变化;测定心肌NOX活性及MDA含量;实时荧光定量PCR测定心肌NOX亚基gp22 phox、gp91 phox mRNA表达;western blotting测定心肌磷酸化PKCδ蛋白表达。结果:PE、DE组心肌发生损伤,但PE组更严重;较运动后24 h的损伤情况,运动后36 h已有明显好转。PE与PC组相比、DE与DC组相比,PE与DE组磷酸化PKCδ蛋白表达、gp22 phox与gp91 phox mRNA表达及NOX的活性、MDA含量等指标水平显著升高(P<0.05),但运动后36 h的水平较运动后24 h已有显著回落(P<0.05);此外,DE组各项指标水平显著低于PE组(P<0.05),DC组除MDA之外的其他指标水平也显著低于PC组(P<0.05)。结论:一次较大强度的力竭性耐力跑运动引起心肌可逆性过氧化损伤。力竭运动激活PKCδ,诱导gp22 phox与gp91 phox mRNA表达而提高NOX活性,催生过量活性氧;这是运动性心肌过氧化损伤的机制之一。
Objective： This study explored the PKCδ / NOX pathway of peroxidation injury of rats＇ myocardium after acute vigorous intensity endurance running. Methods： Sixty male adult SD rats were randomly divided into quiet control group（ C）,placebo and exercise group（ PE）,inhibitor and exercise group（ DE）. According to the experimental design,the group C was randomly divided into placebo and quiet control group（ PC）,inhibitor and quiet control group（ DC）. Rats in DC and DE were intervened by PKCδ specific inhibitor Rottlerin,and rats in PC and PE were used with placebo. Then rats in PE and DE underwent vigorous intensity endurance running to exhaustion. Rats in PE and DE were also separately randomly divided into two groups of 24 h after exercise group,and 36 h after exercise group. The changes of c Tn I,CK-MB levels and myocardial cell ultrastructure were analyzed,NOX activity and MDA content were measured. The mRNA expression of gp22 phox and gp91 phox of NOX subunit were measured by Real-time PCR. Expression of phosphorylated PKCδ protein was measured by Western Blotting. Results： Myocardial injury was found in rats in DE and PE,but it in PE was more serious. Comparedwith 24 h after exercise,the injury of the 36 h after exercise was significantly improved in DE or PE. Compared with group PC or group DE,the phosphorylated PKCδ protein expression,mRNA expression of gp22 phox and gp91 phox,NOX activity and MDA content in PE and DE groups were significantly increased（ P〈0. 05）. But these indicators levels of 36 h after exercise were also significantly lower than those of 24 h after exercise（ P〈 0. 05）. In addition,all the indicators levels of group DE were significantly lower than those of group PE（ P 〈0. 05）. And all these indicators except MDA in group DC were significantly lower than those in group PC（ P 0. 05）. Conclusion： Acute vigorous intensity endurance running to exhaustion can induce reversible peroxidation injury in rats＇ myocardium. Exhaustive excise activates PKCδ,induces gp22 phox and gp91 phox mRNA expression to increase NOX activity,and to produce ROS in excess,which is one of the mechanisms of exercise inducing myocardial peroxidation injury.
出处
《北京体育大学学报》
CSSCI
北大核心
2016年第3期73-80,105,共9页
Journal of Beijing Sport University
基金
广西自然科学基金资助项目(编号:2013GXNSFBA019146)
关键词
力竭运动
PKCΔ
NOX
心肌过氧化损伤
exhaustive exercise
protein kinase Cδ
NOX
myocardial peroxidation injury
