Zhang Ting, Li Xue-Ying, Kuang Dan-Dan, Pan Li-Hua, Li Qiang-Ming, Luo Jian-Ping, Zha Xue-Qiang
Engineering Research Centre of Bioprocess of Ministry of Education, School of Food and Biological Engineering, Hefei University of Technology, No. 193 Tunxi Road, Hefei 230009, People's Republic of China; School of Food and Biological Engineering, Hefei University of Technology, No. 193 Tunxi Road, Hefei 230009, People's Republic of China.
Engineering Research Centre of Bioprocess of Ministry of Education, School of Food and Biological Engineering, Hefei University of Technology, No. 193 Tunxi Road, Hefei 230009, People's Republic of China; School of Food and Biological Engineering, Hefei University of Technology, No. 193 Tunxi Road, Hefei 230009, People's Republic of China.
Int J Biol Macromol. 2025 Mar;296:139706. doi: 10.1016/j.ijbiomac.2025.139706. Epub 2025 Jan 9.
This study aimed to investigate the anti-fatigue efficacy and underlying mechanisms of Polygonatum cyrtonema Hua polysaccharide (PCP) in chronic sleep-deprived mice. Following three weeks of oral administration, PCP demonstrated significant efficacy in alleviating fatigue symptoms. This was evidenced by the prolonged swimming and rotarod time in the high-dose group of PCP, which increased by 73 % and 64 %, respectively. Additionally, serum activities of CAT, GSH-Px, and SOD enzymes rose by 53.56 %, 37.69 % and 53.67 %, respectively, while MDA, lactic acid and BUN levels decreased by 22.90 %, 17.48 % and 24.61 %. The crosstalk between bone and brain is crucial for maintaining energy homeostasis. Molecular docking studies indicated a spontaneous and strong mutual binding between PCP and the bone-promoting target protein BMPR1A. Furthermore, it was observed that PCP enhanced osteogenic differentiation via the BMP-2/Smad1 pathway, leading to an upregulation of osteocalcin expression, which in turn regulated neurotransmitter balance and improved central arousal capacity. Moreover, PCP treatment stimulated neurogenesis by activating the CREB/BDNF/Akt signaling cascade, exhibiting neurotrophic effects. Additionally, PCP increased AMPK phosphorylation and destabilized TXNIP, facilitating astrocyte glucose uptake, glycolysis, and lactate conversion to support neuronal activity. These findings suggested that PCP could effectively respond to energy demands through bone-brain crosstalk, ultimately exerting anti-fatigue properties.
本研究旨在探讨黄精多糖（PCP）对慢性睡眠剥夺小鼠的抗疲劳功效及潜在机制。口服给药三周后，PCP在缓解疲劳症状方面显示出显著功效。PCP高剂量组的小鼠游泳和转棒时间延长，分别增加了73%和64%，这证明了该功效。此外，血清中CAT、GSH-Px和SOD酶的活性分别提高了53.56%、37.69%和53.67%，而MDA、乳酸和BUN水平分别降低了22.90%、17.48%和24.61%。骨与脑之间的相互作用对于维持能量稳态至关重要。分子对接研究表明，PCP与促进骨生成的靶蛋白BMPR1A之间存在自发且强烈的相互结合。此外，观察到PCP通过BMP-2/Smad1途径增强成骨分化，导致骨钙素表达上调，进而调节神经递质平衡并提高中枢唤醒能力。此外，PCP治疗通过激活CREB/BDNF/Akt信号级联反应刺激神经发生，表现出神经营养作用。此外，PCP增加了AMPK磷酸化并使TXNIP不稳定，促进星形胶质细胞摄取葡萄糖、进行糖酵解以及将乳酸转化，以支持神经元活动。这些发现表明，PCP可通过骨-脑相互作用有效应对能量需求，最终发挥抗疲劳特性。
