Abstract：
The anti-inflammatory role of physical exercise is mediated by interleukin 10 (IL-10), and their release is possibly upregulated in response to IL-6. Previous studies demonstrated that mice lacking IL-6 (IL-6 KO mice) exhibited diminished exercise tolerance, and reduced strength. Rev-erbα, a transcriptional suppressor involved in circadian rhythm, has been discovered to inhibit the expression of genes linked to bodily functions, encompassing inflammation and metabolism. It also plays a significant role in skeletal muscle and exercise performance capacity. Given the potential association between Rev-erbα and the immune system and the fact that both pathways are modulated following acute aerobic exercise, we examined the physical performance of IL-10 KO mice and analyzed the modulation of the atrophy and Rev-erbα pathways in the muscle of wild type (WT) and IL-10 KO mice following one session of acute exercise. For each phenotype, WT and IL-10 KO were divided into two subgroups (Control and Exercise). The acute exercise session started at 6 m/min, followed by 3 m/min increments every 3 min until animal exhaustion. Two hours after the end of the exercise protocol, the gastrocnemius muscle was removed and prepared for the reverse transcription-quantitative polymerase chain reaction (RT-q-PCR) and immunoblotting technique. In summary, compared to WT, the IL-10 KO animals showed lower body weight and grip strength in the baseline. The IL-10 control group presented a lower protein content of BMAL1. After the exercise protocol, the IL-10 KO group had higher mRNA levels of Trim63 (atrophy signaling pathway) and lower mRNA levels of Clock and Bmal1 (Rev-erbα signaling pathway). This is the first study showing the relationship between Rev-erbα and atrophy in IL-10 KO mice. Also, we accessed a public database that analyzed the gastrocnemius of MuRF KO mice submitted to two processes of muscle atrophy, a denervation surgery and dexamethasone (Dexa) injections. Independently of knockout, the denervation demonstrated lower Nr1d1 levels. In conclusion, IL-10 seems to be a determinant in the Rev-erbα pathway and atrophy after acute exercise, with no modulation in the baseline state.
摘要：
体育锻炼的抗炎作用是由白细胞介素10（IL-10）介导的，并且它们的释放可能在响应IL-6时上调。先前的研究表明，缺乏IL-6的小鼠（IL-6KO小鼠）表现出运动耐量降低，强度降低。Rev-erbα,参与昼夜节律的转录抑制因子，已经发现抑制与身体功能相关的基因的表达，包括炎症和新陈代谢。它在骨骼肌和运动表现能力方面也起着重要作用。考虑到Rev-erbα与免疫系统之间的潜在关联，以及两种途径在急性有氧运动后受到调节的事实，我们检查了IL-10KO小鼠的身体表现，并分析了一次急性运动后野生型（WT）和IL-10KO小鼠肌肉中萎缩和Rev-erbα途径的调节。对于每种表型，WT和IL-10KO分为两个亚组(对照和运动)。急性锻炼以6米/分钟的速度开始，然后每3分钟增加3米/分钟，直到动物筋疲力尽。锻炼方案结束两小时后,取腓肠肌,准备逆转录-定量聚合酶链反应(RT-q-PCR)和免疫印迹技术.总之,与WT相比，IL-10KO动物在基线显示较低的体重和握力。IL-10对照组呈现较低的BMAL1蛋白含量。在锻炼方案之后，IL-10KO组Trim63(萎缩信号通路)mRNA水平较高,Clock和Bmal1(Rev-erbα信号通路)mRNA水平较低.这是第一个显示IL-10KO小鼠中Rev-erbα与萎缩之间关系的研究。此外，我们访问了一个公共数据库，该数据库分析了MuRFKO小鼠的腓肠肌，去神经支配手术和地塞米松（Dexa）注射。独立于淘汰赛，神经支配显示Nr1d1水平较低。总之,IL-10似乎是Rev-erbα途径和急性运动后萎缩的决定因素，在基线状态没有调制。
