Department of Exercise Science, High Point University, One University Parkway, High Point, NC, 27268, USA.
Department of Kinesiology, California Baptist University, Riverside, CA, 92504, USA.
Eur J Appl Physiol. 2018 Dec;118(12):2707-2717. doi: 10.1007/s00421-018-3998-5. Epub 2018 Oct 1.
Curcumin reduces gut barrier damage and plasma cytokine responses to exertional heat stress. However, the role of peripheral blood mononuclear cell (PBMC) in this response remains unclear.
This work investigated the effect of 3 days of 500 mg/day dietary curcumin supplementation on PBMC responses to exertional heat stress in non-heat acclimated humans.
Eight participants ran (65% VO) for 60 min in an environmental chamber (37 °C/25% RH) two times (curcumin/placebo). Blood samples were collected pre, post, 1 h post, and 4 h post-exercise. PBMC were isolated from blood samples and the protein content of markers along the TLR4 signaling pathway (TLR4, MyD88, pNF-κB, NF-κB), indicators of cellular energy status (SIRT1 and p-AMPK), and mediators of cellular heat shock response (pHSF-1 and HSP70) were examined with Western blot. Data were analyzed with two-way (condition × time) RM-ANOVAs with Newman-Keuls post hocs.
As compared to placebo, curcumin did not alter protein expression in PBMC (p > 0.05). However, in both study conditions at 1 h post-reductions were noted in TLR 4 (- 21.5%; p = 0.03), HSP70 (- 11.0%; p = 0.04), pAMPK (- 48.5%; p < 0.01), and SIRT1 (- 47.8%; p < 0.01). Remarkably, the ratio of pNF-κB to NF-κB was elevated in both conditions at this same timepoint (+ 75.4%; p = 0.02).
Inflammatory protein expression in PBMC did not differ between curcumin and placebo conditions. Downregulation of pAMPK/SIRT1 and release of HSP70 to the bloodstream may compensate for reduced TLR4, allowing PBMC to maintain inflammatory capacity and preventing an "open window" during the hours following hyperthermic exercise.
姜黄素可减轻肠道屏障损伤和血浆细胞因子对运动性热应激的反应。然而，外周血单个核细胞（PBMC）在此反应中的作用尚不清楚。
本研究旨在探讨 3 天 500mg/天饮食姜黄素补充对非热适应人体运动性热应激时 PBMC 反应的影响。
8 名参与者在环境室（37°C/25%RH）中以 65% VO 跑步 60min，两次（姜黄素/安慰剂）。在运动前、运动后、运动后 1 小时和运动后 4 小时采集血液样本。从血液样本中分离 PBMC，并使用 Western blot 检测 TLR4 信号通路（TLR4、MyD88、pNF-κB、NF-κB）、细胞能量状态标志物（SIRT1 和 p-AMPK）和细胞热休克反应介质（pHSF-1 和 HSP70）的蛋白含量。数据采用双因素（条件×时间）重复测量方差分析和 Newman-Keuls 事后检验进行分析。
与安慰剂相比，姜黄素并未改变 PBMC 中的蛋白表达（p>0.05）。然而，在两种研究条件下，运动后 1 小时，TLR4 减少了-21.5%（p=0.03），HSP70 减少了-11.0%（p=0.04），pAMPK 减少了-48.5%（p<0.01），SIRT1 减少了-47.8%（p<0.01）。值得注意的是，在同一时间点，两种情况下 pNF-κB/NF-κB 的比值均升高（+75.4%，p=0.02）。
姜黄素和安慰剂条件下 PBMC 的炎症蛋白表达无差异。pAMPK/SIRT1 的下调和 HSP70 向血液中的释放可能补偿 TLR4 的减少，使 PBMC 保持炎症能力，并防止热应激后数小时内出现“开放窗口”。
