Habitual physical activity facilitates stress-induced HSP72 induction in brain, peripheral, and immune tissues
Habitual physical activity facilitates stress-induced HSP72 induction in brain, peripheral, and immune tissues
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DOI：
10.1152/ajpregu.00513.2002
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发表时间：
2003-02-01
影响因子：
2.8
通讯作者：
Fleshner, M
中科院分区：
文献类型：
--
作者：
Campisi, J;Leem, TH;Fleshner, M
身体活跃的生物体如何抵抗急性应激源暴露的许多破坏性影响的机制尚不清楚。细胞诱导热休克蛋白（例如，HSP72）是一种成功的策略，用于细胞在应激的破坏性影响中生存。因此，体力活动的应激缓冲作用可能是由于HSP72对应激反应的改善。因此，本研究的目的是确定先前的自愿自由跑是否促进应激诱导的中枢（脑）、外周和免疫组织中HSP72的诱导。在应激源暴露前，成年雄性Fischer 344大鼠被安置在一个移动的跑步轮（Active）或一个锁定的不移动的跑步轮（Sed）中8周。大鼠暴露于不可避免的尾震应激（IS； 100次1.6 ma尾震，持续5秒，间隔60秒），穷尽性运动应激（EXS；跑步机跑到精疲力竭）或无应激（对照组）。应激源终止后2小时采集血液、脑和周围组织。在培养的肠系膜淋巴结细胞中测定IS诱导HSP72的动力学。通过测定血清皮质酮（RIA）来验证应激反应的激活。用HSP72 ELISA法测定细胞裂解液中组织和细胞HSP72的含量。应激后，Active和Sed大鼠血清皮质酮水平均升高。相比之下，暴露于IS和/或EXS的活性大鼠而非Sed大鼠的背迷走神经复合体、额叶皮质、海马、垂体、肾上腺、肝脏、脾脏、肠系膜淋巴结和心脏的HSP72升高。此外，与Sed大鼠相比，暴露于IS的Active大鼠表现出更快的淋巴细胞HSP72诱导。因此，与Sed大鼠相比，Active大鼠对应激的HSP72反应更大、更快。这些结果表明，先前的体育活动增强了HSP72在各种应激源后的表达。促进HSP72的诱导可能有助于提高身体活跃的生物体的抗逆性。
The mechanism( s) for how physically active organisms are resistant to many damaging effects of acute stressor exposure is unknown. Cellular induction of heat-shock proteins (e. g., HSP72) is one successful strategy used by the cell to survive the damaging effects of stress. It is possible, therefore, that the stress-buffering effect of physical activity may be due to an improved HSP72 response to stress. Thus the purpose of the current study was to determine whether prior voluntary freewheel running facilitates the stress-induced induction of HSP72 in central (brain), peripheral, and immune tissues. Adult male Fischer 344 rats were housed with either a mobile running wheel (Active) or a locked, immobile wheel [sedentary (Sed)] for 8 wk before stressor exposure. Rats were exposed to either inescapable tail-shock stress (IS; 100 1.6-mA tail shocks, 5-s duration, 60-s intertrial interval), exhaustive exercise stress (EXS; treadmill running to exhaustion), or no stress (controls). Blood, brain, and peripheral tissues were collected 2 h after stressor termination. The kinetics of HSP72 induction after IS was determined in cultured mesenteric lymph node cells. Activation of the stress response was verified by measuring serum corticosterone (RIA). Tissue and cellular HSP72 content were measured using HSP72 ELISA in cell lysates. Both Active and Sed rats had elevated levels of serum corticosterone after stress. In contrast, Active but not Sed rats exposed to IS and/or EXS had elevated HSP72 in dorsal vagal complex, frontal cortex, hippocampus, pituitary, adrenal, liver, spleen, mesenteric lymph nodes, and heart. In addition, Active rats exposed to IS demonstrated a faster induction of lymphocyte HSP72 compared with Sed rats. Thus Active rats responded to stress with both greater and faster HSP72 responses compared with Sed rats. These results indicate that previous physical activity potentiates HSP72 expression after a wide range of stressors. Facilitated induction of HSP72 may contribute to the increased stress resistance previously reported in physically active organisms.