Forced treadmill exercise training exacerbates inflammation and causes mortality while voluntary wheel training is protective in a mouse model of colitis.
Forced treadmill exercise training exacerbates inflammation and causes mortality while voluntary wheel training is protective in a mouse model of colitis.
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DOI：
10.1016/j.bbi.2013.05.005
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发表时间：
2013-10
期刊：
影响因子：
--
通讯作者：
Woods JA
中科院分区：
文献类型：
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作者：
Cook MD;Martin SA;Williams C;Whitlock K;Wallig MA;Pence BD;Woods JA
这项研究的目的是检查运动训练是否减少了结肠炎小鼠模型的炎症和症状。我们假设，适度的强制跑步机跑步(FTR)或自愿车轮跑步(VWR)可以减少葡聚糖硫酸钠(DSS)引起的结肠炎症状和结肠炎。雄性C57BL/6J小鼠随机分为静坐、中等强度FTR(8~12m/min，40min，6周，5x/周)和VWR(30天接触轮子)。在饮水中加入2%(w/v)的DSS，持续5d。在DSS治疗前和治疗期间，小鼠停止运动。分别于FTR的第6、8、12天和VWR实验的第8天采集结肠。与我们的假设相反，我们发现适度的FTR加剧了结肠炎的症状和炎症，表现为腹泻和IL-6、IL-1β、IL-17结肠基因表达的显著增加(p<0.05)。我们还观察到FTR/DSS组的死亡率更高(3/10死亡比0/10，p=0.07)。相反，VWR减轻了DSS治疗组小鼠的结肠炎症状，减少了结肠炎性基因的表达(p≤0.05)。虽然DSS治疗减少了食物/水的摄入量和体重，但FTR有恶化的趋势，而VWR则减弱这种影响。FTR(在没有DSS的情况下)增加了趋化因子和抗菌蛋白CCL6的基因表达，这表明FTR改变了肠道的稳态，这可能与对DSS的夸大反应有关。总之，我们发现DSS导致FTR加重，而VWR减轻，症状和炎症反应减轻。
The purpose of this study was to examine whether exercise training reduced inflammation and symptomology in a mouse model of colitis. We hypothesized that moderate forced treadmill running (FTR) or voluntary wheel running (VWR) would reduce colitis symptoms and colon inflammation in response to dextran sodium sulfate (DSS). Male C57Bl/6J mice were randomized to sedentary, moderate intensity FTR (8–12 m/min, 40 min, 6 weeks, 5x/week), or VWR (30 days access to wheels). DSS was given at 2% (w/v) in drinking water over 5 days. Mice discontinued exercise 24 h prior to and during DSS treatment. Colons were harvested on Days 6, 8 and 12 in FTR and Day 8 post-DSS in VWR experiments. Contrary to our hypothesis, we found that moderate FTR exacerbated colitis symptomology and inflammation as measured by significant (p≤0.05) increases in diarrhea and IL-6, IL-1β, IL-17 colon gene expression. We also observed higher mortality (3/10 died vs. 0/10, p = 0.07) in the FTR/DSS group. In contrast, VWR alleviated colitis symptoms and reduced inflammatory gene expression in the colons of DSS-treated mice (p≤0.05). While DSS treatment reduced food/fluid intake and body weight, there was a tendency for FTR to exacerbate, and for VWR to attenuate, this effect. FTR (in the absence of DSS) increased gene expression of the chemokine and antibacterial protein CCL6 suggesting that FTR altered gut homeostasis that may be related to the exaggerated response to DSS. In conclusion, we found that FTR exacerbated, whereas VWR attenuated, symptoms and inflammation in response to DSS.