<p>Moderate sports training help to enhance spleen-mediated immune function, while prolonged and high-intensity physical exercises could produce an opposite effect. The specific mechanisms underlying the effects of physical load on apoptosis of splenic lymphocytes remain unclear. To address this gap, we developed a model of physical exercises in rats in order to explore the effect of intensity of these exercises on splenic lymphocyte apoptosis and its potential mechanism. We found that high-intensity exercises reduced the CD4<sup>+</sup>/CD8<sup>+</sup> ratio, increased oxidative stress and mitochondrial membrane potential levels, activated NLRP3 inflammasomes, and promoted the expression of proapoptotic proteins, but decreased expression of anti-apoptotic proteins. In contrast, the moderate exercises produced no significant changes in ROS and mitochondrial membrane potential levels, while exerting the opposite effects on other parameters specifies in the above in comparison with the effects observed in rats subjected to intensive physical load. These results suggest that the high-intensity physical exercises promote lymphocyte apoptosis by excessive ROS release and activation of NLRP3 inflammasomes.</p>

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Aerobic Exercise Affected Lymphocyte Apoptosis by Modulating ROS Release and NLRP3 Inflammasome Activation

  • X. Lian,
  • Z. Guo,
  • J. Liu,
  • W. Zeng

摘要

Moderate sports training help to enhance spleen-mediated immune function, while prolonged and high-intensity physical exercises could produce an opposite effect. The specific mechanisms underlying the effects of physical load on apoptosis of splenic lymphocytes remain unclear. To address this gap, we developed a model of physical exercises in rats in order to explore the effect of intensity of these exercises on splenic lymphocyte apoptosis and its potential mechanism. We found that high-intensity exercises reduced the CD4+/CD8+ ratio, increased oxidative stress and mitochondrial membrane potential levels, activated NLRP3 inflammasomes, and promoted the expression of proapoptotic proteins, but decreased expression of anti-apoptotic proteins. In contrast, the moderate exercises produced no significant changes in ROS and mitochondrial membrane potential levels, while exerting the opposite effects on other parameters specifies in the above in comparison with the effects observed in rats subjected to intensive physical load. These results suggest that the high-intensity physical exercises promote lymphocyte apoptosis by excessive ROS release and activation of NLRP3 inflammasomes.