Department of Rehabilitation, Hengyang Medical School, The First Affiliated Hospital, University of South China, No. 69, Chuanshan Road, Hengyang, Hunan Province, 421001, Hengyang, People's Republic of China.
Rehabilitation Laboratory, Hengyang Medical School, The First Affiliated Hospital, University of South China, 421001, Hengyang, Hunan, China.
BMC Musculoskelet Disord. 2022 Dec 13;23(1):1089. doi: 10.1186/s12891-022-06055-5.
Although aerobic physical exercise may improve osteoporosis during ageing, the underlying mechanism of the favorable effects remains unclear. The aim of this study was to examine the localized and generalized proinflammatory indicators and the adaptive skeletal responses to treadmill training in aged rats to explore the potential mechanisms by which treadmill training impacts bone deterioration in a natural aged rat model.
A total of 24 Sprague Dawley (SD) rats were included in this study. Sixteen of all these animals were twenty-four months natural aged male SD rats, which were distributed into two groups (n = 8/group): AC group with sham treadmill training, and AT group with 8 weeks treadmill training. The remaining 8 were six months male SD rats matched subline and supplier, which were used as the adult control group with sham treadmill training (YC group, n = 8). The serum, bone marrow, fresh femur, tibia, and lumbar spine were harvested for molecular biological analysis, bone mineral density (BMD) testing, and micro-CT analysis after 8 weeks of treadmill training.
After 8 weeks of intervention, the results showed that treadmill training increased BMD and inhibited deterioration of bone microarchitecture of hind limb bones. Further analysis showed that treadmill training increased serum P1CP concentration and decreased serum CTX-1level. Interestingly, treadmill training down-regulated the protein expressions of proinflammatory indicators, including NLRP3, proCaspase1, cleaved Caspase1, IL-1β, and GSDMD-N, and the mRNA levels of NLRP3, Caspase1, and IL-1β of the bone marrow. In addition, treadmill training also inhibited serum TNF-α and IL-1β concentration. However, 8 weeks of treadmill training did not increase BMD and bone microarchitecture in the lumbar spine.
Treadmill training mitigates the ageing-induced bone loss and reverses the deterioration of bone microarchitecture in hind limbs probably through inhibiting NLRP3/Caspase1/IL-1β signaling to attenuate low-grade inflammation and improve the inflammatory bone microenvironment.
尽管有氧运动可能会改善衰老过程中的骨质疏松症，但尚不清楚其有益作用的潜在机制。本研究旨在检测跑步机训练对老年大鼠局部和全身性促炎指标以及适应性骨骼反应，以探讨跑步机训练对自然衰老大鼠模型中骨恶化的潜在影响机制。
本研究共纳入 24 只 Sprague Dawley（SD）大鼠。所有这些动物中，有 16 只为 24 个月龄的自然衰老雄性 SD 大鼠，将其分为两组（每组 8 只）：AC 组接受假跑步机训练，AT 组接受 8 周跑步机训练。其余 8 只为 6 个月龄雄性 SD 大鼠，来自同一供应商，作为成年对照组，接受假跑步机训练（YC 组，n=8）。8 周跑步机训练后，采集血清、骨髓、新鲜股骨、胫骨和腰椎进行分子生物学分析、骨密度（BMD）检测和 micro-CT 分析。
干预 8 周后，结果显示跑步机训练增加了 BMD，抑制了后肢骨骨微结构的恶化。进一步分析表明，跑步机训练增加了血清 P1CP 浓度，降低了血清 CTX-1 水平。有趣的是，跑步机训练下调了骨髓中促炎指标 NLRP3、proCaspase1、cleaved Caspase1、IL-1β 和 GSDMD-N 的蛋白表达，以及 NLRP3、Caspase1 和 IL-1β 的 mRNA 水平。此外，跑步机训练还抑制了血清 TNF-α 和 IL-1β 浓度。然而，8 周的跑步机训练并没有增加腰椎的 BMD 和骨微结构。
跑步机训练减轻了衰老引起的骨丢失，并逆转了后肢骨微结构的恶化，可能是通过抑制 NLRP3/Caspase1/IL-1β 信号通路来减轻低度炎症并改善炎症性骨微环境。
