Role of NF-κB-p65, ICAM-1 and apoptosis in exhausted exercise-induced delayed-onset myocardial injury

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.