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NF-κB-p65、ICAM-1和细胞凋亡在力竭性运动诱发延迟性心肌损伤中的作用

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2013年第2期
页码:
172-175189
栏目:
基础研究
出版日期:
2013-04-25

文章信息/Info

Title:
Role of NF-κB-p65, ICAM-1 and apoptosis in exhausted exercise-induced delayed-onset myocardial injury
作者:
王春晓1; 梁玉记1; 王 燕1; 胡志力1; 王福文1; 2
(1.山东省医学科学院药物研究所、济南大学山东省医学科学院医学与生命科学学院，山东 济南 250062；2.山东省罕少见病重点实验室，山东 济南 250062)
Author(s):
WANG Chun-xiao1;  LIANG Yu-ji1;  WANG Yan1;  HU Zhi-li1;  WANG Fu-wen1; 2
(1.Institute of Materia Medica, Shandong Academy of Medical Sciences & School of Medicine and Life Sciences, Shandong Academy of Medical Sciencesr, University of Jinan, Jinan 250062, Shandong, China; 2.Shandong Provincial Key Laboratory for Rare Diseases, Jinan 250062, Shandong, China)
关键词:
力竭性运动; 心肌损伤; 核转录因子-κB-p65; 细胞间黏附因子-1; 细胞凋亡; 大鼠
Keywords:
exhaustive exercise;  myocardial injury;  nuclear transcription factor-kappa B;  intracellular adhesion molecule-1;  apoptosis;  rats
分类号:
R873
DOI:
-
文献标识码:
A
摘要:
目的:观察反复力竭性游泳运动后，不同时相大鼠心肌组织中核转录因子-κB（NF-κB）-p65、细胞间黏附因子-1（ICAM-1）和细胞凋亡的动态变化，以评价在运动延迟性心肌损伤中的作用。方法: 采用反复力竭性游泳运动建立延迟性心肌损伤大鼠模型。将无训练的80只Wistar雄性大鼠随机分为安静对照组和反复力竭性运动后即刻组、3 h组、6 h组、12 h组、24 h组、48 h组和96 h组。每组10只大鼠(n=10)。分别于末次运动后即刻、3、6、12、24、48 h和96 h快速取出心脏，应用免疫组化染色法和DNA原位末端标记（TUNEL）法检测大鼠心肌组织中NF-κB-p65和ICAM-1表达的水平和细胞凋亡的动态变化。结果: 与安静对照组比较，反复力竭性运动后不同时相大鼠心肌细胞中NF-κB-p65和ICAM-1蛋白的表达及细胞凋亡指数均显著增加（分别为P<0.05和P<0.01），其中心肌细胞中NF-κB-p65的表达和细胞凋亡于运动后48 h达高峰，ICAM-1蛋白的表达于运动后即刻达高峰，运动后96 h有所减轻。结论: 反复力竭性运动可以造成早期心肌缺血缺氧损伤，刺激心肌细胞中NF-κB-p65和ICAM-1表达的水平的升高，促进炎症反应，并诱导心肌细胞凋亡，进一步加重运动后早期心肌损伤，诱发延迟性心肌损伤。
Abstract:
AIM:To investigate the dynamic changes of nuclear transcription factor-kappa B (NF-κB)p65, intracellular adhesion molecule-1 (ICAM-1) and apoptosis in myocardium of rats at different time periods after repeated exhausted exercise and to explore their roles in the development of exercise-induced delayed-onset myocardial injury. METHODS: The animal model of delayed-onset myocardial injury was established by repeated exhaustive swimming. Eighty male Wistar rats were divided randomly into sedentary control group and exhausted exercise groups, namely, 3-, 6-, 12-, 24-, 48- and 96-h groups. Rat hearts were rapidly excised at respective time points of 3-, 6-, 12-, 24-, 48- and 96-h immediately after the exhausted exercise. The expressions of NF-κB-p65 and ICAM-1 proteins were detected by immunohistochemical staining and apoptotic cells were assayed by TUNEL method. RESULTS: Compared with those rats in the sedentary control group, the expressions of NF-κB-p65 and ICAM-1 proteins and apoptosis indexes in rat myocardium significantly increased at different time periods after repeated exhaustive exercise (P<0.05 and P<0.01). The expressions of NF-κB-p65 and apoptosis peaked at 48 h and ICAM-1 proteins peaked at the time points immediately after exercise and decreased at 96 h post-exercise. CONCLUSION: The hypoxic-ischemic rat myocardial damage induced by repeated exhaustive exercise could lead to high expressions of NF-κB-p65 and ICAM-1, which promotes the inflammatory responses and apoptosis of myocytes and further aggravates early myocardial injury, resulting in exercise-induced delayed-onset myocardial injury.

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备注/Memo

备注/Memo:
收稿日期：2012-08-19.基金项目：山东省自然科学基金项目资助（ZR2009CM089） 通讯作者：王福文，研究员，主要从事心脑血管生理药理研究 Email：wangfuwww@tom.com 作者简介：王春晓，硕士生 Email：wangchunxiao1988@126.com
更新日期/Last Update: 2013-04-28