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布洛芬补充剂及其对阻力运动后骨骼肌中核因子κB激活的影响。

Ibuprofen supplementation and its effects on NF-κB activation in skeletal muscle following resistance exercise.

作者信息

Vella Luke, Markworth James F, Peake Jonathan M, Snow Rod J, Cameron-Smith David, Russell Aaron P

机构信息

Centre for Physical Activity and Nutrition, School of Exercise and Nutrition Science, Deakin University, Burwood, Vic., Australia.

Liggins Institute, University of Auckland, Auckland, New Zealand.

出版信息

Physiol Rep. 2014 Oct 24;2(10). doi: 10.14814/phy2.12172. Print 2014 Oct 1.

Abstract

Resistance exercise triggers a subclinical inflammatory response that plays a pivotal role in skeletal muscle regeneration. Nuclear factor-κB (NF-κB) is a stress signalling transcription factor that regulates acute and chronic states of inflammation. The classical NF-κB pathway regulates the early activation of post-exercise inflammation; however there remains scope for this complex transcription factor to play a more detailed role in post-exercise muscle recovery. Sixteen volunteers completed a bout of lower body resistance exercise with the ingestion of three 400 mg doses of ibuprofen or a placebo control. Muscle biopsy samples were obtained prior to exercise and at 0, 3 and 24 h post-exercise and analysed for key markers of NF-κB activity. Phosphorylated p65 protein expression and p65 inflammatory target genes were elevated immediately post-exercise independent of the two treatments. These changes did not translate to an increase in p65 DNA binding activity. NF-κB p50 protein expression and NF-κB p50 binding activity were lower than pre-exercise at 0 and 3 h post-exercise, but were elevated at 24 h post-exercise. These findings provide novel evidence that two distinct NF-κB pathways are active in skeletal muscle after resistance exercise. The initial wave of activity involving p65 resembles the classical pathway and is associated with the onset of an acute inflammatory response. The second wave of NF-κB activity comprises the p50 subunit, which has been previously shown to resolve an acute inflammatory program. The current study showed no effect of the ibuprofen treatment on markers of the NF-κB pathway, however examination of the within group effects of the exercise protocol suggests that this pathway warrants further research.

摘要

抗阻运动引发一种亚临床炎症反应,该反应在骨骼肌再生中起关键作用。核因子-κB(NF-κB)是一种应激信号转录因子,可调节炎症的急性和慢性状态。经典的NF-κB途径调节运动后炎症的早期激活;然而,这种复杂的转录因子在运动后肌肉恢复中发挥更详细作用的空间仍然存在。16名志愿者在摄入三剂400毫克布洛芬或安慰剂对照的情况下完成了一轮下肢抗阻运动。在运动前以及运动后0、3和24小时采集肌肉活检样本,并分析NF-κB活性的关键标志物。运动后立即观察到磷酸化p65蛋白表达和p65炎症靶基因升高,且与两种治疗方法无关。这些变化并未转化为p65 DNA结合活性的增加。运动后0和3小时,NF-κB p50蛋白表达和NF-κB p50结合活性低于运动前,但在运动后24小时升高。这些发现提供了新的证据,表明抗阻运动后骨骼肌中有两条不同的NF-κB途径被激活。涉及p65的初始活动浪潮类似于经典途径,并与急性炎症反应的开始有关。NF-κB活动的第二波由p50亚基组成,此前已证明该亚基可解决急性炎症程序。目前的研究表明布洛芬治疗对NF-κB途径的标志物没有影响,然而,对运动方案组内效应的检查表明,该途径值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95a3/4254097/053c989a6210/phy2-2-e12172-g1.jpg

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