力竭运动对人外周血单核细胞炎症、凋亡和抗氧化信号通路的影响。

IF 2.5 Q3 ONCOLOGY
Si-Young Kim, Young-Joon Surh, Young-Soo Lee
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引用次数: 0

摘要

在本研究中,我们研究了穷尽性运动和恢复对人外周血单核细胞(PBMCs)炎症、促凋亡和抗氧化反应的影响。16名志愿者参加了一个有指导的体育活动项目,在这个项目中,他们在跑步机上进行渐进式运动,直到精疲力竭,然后是1小时的恢复期。分别在运动前、运动后和恢复1小时后采集分离的人外周血单核细胞。力竭运动诱导血红素加氧酶-1和谷氨酸半胱氨酸连接酶催化亚基的表达和NF-κB和NF- e2相关因子2 (Nrf2)的激活。caspase-3及其底物PARP的活性和裂解程度也显著增加。然而,诱导氧化还原信号和促凋亡反应在1小时恢复期间完全恢复到基线水平。另一方面,在1小时的恢复期,停止运动后COX-2表达持续升高。考虑到所有这些发现,我们得出结论,穷尽性运动短暂地诱导nrf2介导的抗氧化基因表达,并通过凋亡消除受损细胞,作为抗氧化和炎症应激的适应性细胞保护反应的一部分。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Effects of Exhaustive Exercise on Inflammatory, Apoptotic, and Antioxidative Signaling Pathways in Human Peripheral Blood Mononuclear Cells.

Effects of Exhaustive Exercise on Inflammatory, Apoptotic, and Antioxidative Signaling Pathways in Human Peripheral Blood Mononuclear Cells.

Effects of Exhaustive Exercise on Inflammatory, Apoptotic, and Antioxidative Signaling Pathways in Human Peripheral Blood Mononuclear Cells.

Effects of Exhaustive Exercise on Inflammatory, Apoptotic, and Antioxidative Signaling Pathways in Human Peripheral Blood Mononuclear Cells.

In the present study, we investigated the effects of exhaustive exercise and recovery on inflammatory, pro-apoptotic, and anti-oxidative responses in human peripheral blood mononuclear cells (PBMCs). Sixteen volunteers participated in a guided physical activity program in which they were subjected to progressive exercise on the treadmill until they were exhausted followed by an 1-hour recovery period. Isolated human PBMCs were collected before exercise, immediately after exercise, and after 1-hour recovery. Exhaustive exercise induced expression of heme oxygenase-1 and glutamate cysteine ligase catalytic subunit and activation of NF-κB and NF-E2 related factor 2 (Nrf2). Apoptosis, as measured by activity and cleavage of caspase-3 and its substrate PARP also significantly increased. However, induction of redox signaling and the pro-apoptotic response fully returned to the baseline level during the 1-hour recovery period. On the other hand, COX-2 expression was continuously elevated after exercise cessation throughout the 1-hour recovery period. Taking all these findings into account, we conclude that exhaustive exercise transiently induces Nrf2-mediated antioxidant gene expression and eliminates damaged cells through apoptosis as part of an adaptive cytoprotective response against oxidative and inflammatory stress.

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