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Objective <p>To evaluate the protective effects of aerobic exercise (AE) on cardiac function and myocardial injury in rats with myocardial infarction (MI), as well as its impact on macrophage polarization.</p> Methods <p>A rat model of chronic post-infarction remodeling was established by ligation of the left anterior descending coronary artery, while the Sham group underwent threading without ligation. After a 4-week recovery period, rats in the exercise group underwent an 8-week aerobic training program, with all assessments performed at approximately 12 weeks after MI induction. The maximal aerobic velocity test was performed to assess changes in exercise endurance. To evaluate cardiac architecture, inflammatory infiltrates, and the extent of fibrosis, we performed standard histological staining with hematoxylin-eosin and Masson’s trichrome. Triphenyltetrazolium chloride staining was applied to distinguish infarcted and viable myocardial regions. Commercial assay kits were used to detect myocardial injury markers, inflammatory cytokines, and oxidative stress indicators in myocardial tissue or serum. Western blotting and immunofluorescence staining were performed to assess macrophage polarization.</p> Results <p>AE markedly improved cardiac function in MI rats. It also attenuated MI size and fibrosis. Serum levels of cardiac damage-associated biomarkers (cTnI, CK-MB, and LDH) were significantly decreased following AE, suggesting attenuation of ongoing myocardial injury and adverse remodeling in the chronic post-infarction setting, as were pro-inflammatory cytokines and oxidative stress indicators. Anti-inflammatory and antioxidant capacity were also enhanced by AE. M1 macrophage markers were reduced, along with upregulation of M2 macrophage markers in the myocardial tissue after AE.</p> Conclusion <p>Moderate-intensity AE alleviates myocardial injury, inflammation, and oxidative stress, and promotes macrophage polarization toward the M2 phenotype in rats with MI. These findings may provide evidence for exercise-based rehabilitation and immune-targeted therapeutic strategies.</p>

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Aerobic exercise modulates macrophage polarization and promotes cardiac recovery after myocardial infarction in rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月24日

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  • Mingyan Zhu,
  • Bing Zhou,
  • Jianye Peng,
  • Kong Chen,
  • Yu Wang,
  • Hao Zeng,
  • Xia Zhang

摘要

Objective

To evaluate the protective effects of aerobic exercise (AE) on cardiac function and myocardial injury in rats with myocardial infarction (MI), as well as its impact on macrophage polarization.

Methods

A rat model of chronic post-infarction remodeling was established by ligation of the left anterior descending coronary artery, while the Sham group underwent threading without ligation. After a 4-week recovery period, rats in the exercise group underwent an 8-week aerobic training program, with all assessments performed at approximately 12 weeks after MI induction. The maximal aerobic velocity test was performed to assess changes in exercise endurance. To evaluate cardiac architecture, inflammatory infiltrates, and the extent of fibrosis, we performed standard histological staining with hematoxylin-eosin and Masson’s trichrome. Triphenyltetrazolium chloride staining was applied to distinguish infarcted and viable myocardial regions. Commercial assay kits were used to detect myocardial injury markers, inflammatory cytokines, and oxidative stress indicators in myocardial tissue or serum. Western blotting and immunofluorescence staining were performed to assess macrophage polarization.

Results

AE markedly improved cardiac function in MI rats. It also attenuated MI size and fibrosis. Serum levels of cardiac damage-associated biomarkers (cTnI, CK-MB, and LDH) were significantly decreased following AE, suggesting attenuation of ongoing myocardial injury and adverse remodeling in the chronic post-infarction setting, as were pro-inflammatory cytokines and oxidative stress indicators. Anti-inflammatory and antioxidant capacity were also enhanced by AE. M1 macrophage markers were reduced, along with upregulation of M2 macrophage markers in the myocardial tissue after AE.

Conclusion

Moderate-intensity AE alleviates myocardial injury, inflammation, and oxidative stress, and promotes macrophage polarization toward the M2 phenotype in rats with MI. These findings may provide evidence for exercise-based rehabilitation and immune-targeted therapeutic strategies.