Parkinson's disease (PD) is a common neurodegenerative disease. Damage to energy metabolism and reduced adenosine triphosphate (ATP) levels in dopaminergic neurons are common features of PD. Previous studies suggested that the occurrence of PD often affects glucose metabolism and ATP production in the brain, and increased glycolysis or ATP production protects dopaminergic neuronal degeneration in the brain of PD patients. These systems may provide new potential therapeutic targets for the prevention of PD. The present study investigated the inhibitory action of polydatin (PLD) on early dopaminergic neuronal degeneration induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The results showed that PLD protected against MPTP-induced early dopaminergic neuronal degeneration. PLD reduced the MPTP-induced loss of dopaminergic neurons in substantia nigra and striatum, inhibited the occurrence of neural apoptosis, and restored motor function in mice. PLD also increased the continuous activity duration and rhythm amplitude in mice during the circadian activity test. PLD improved glucose metabolism in the brain and restored ATP production levels. These observations suggest that PLD attenuates MPTP-induced early PD-like symptoms, and its mechanism of action may be associated with the promotion of glucose metabolism in neurons.

帕金森病（PD）是一种常见的神经退行性疾病。能量代谢受损和多巴胺能神经元中三磷酸腺苷 (ATP) 水平降低是 PD 的常见特征。以往的研究表明，PD的发生往往会影响大脑中的葡萄糖代谢和ATP的产生，而糖酵解或ATP产生的增加保护了PD患者大脑中的多巴胺能神经元变性。这些系统可能为预防 PD 提供新的潜在治疗靶点。本研究调查虎杖苷 (PLD) 对 1-甲基-4-苯基-1,2,3,6-四氢吡啶 (MPTP) 诱导的早期多巴胺能神经元变性的抑制作用。结果表明，PLD 可防止 MPTP 诱导的早期多巴胺能神经元变性。PLD减少了MPTP诱导的黑质和纹状体中多巴胺能神经元的丢失，抑制了神经细胞凋亡的发生，恢复了小鼠的运动功能。在昼夜节律活动测试期间，PLD 还增加了小鼠的连续活动持续时间和节律幅度。PLD 改善了大脑中的葡萄糖代谢并恢复了 ATP 生产水平。这些观察结果表明，PLD减轻了MPTP诱导的早期PD样症状，其作用机制可能与促进神经元葡萄糖代谢有关。PLD 改善了大脑中的葡萄糖代谢并恢复了 ATP 生产水平。这些观察结果表明，PLD减轻了MPTP诱导的早期PD样症状，其作用机制可能与促进神经元葡萄糖代谢有关。PLD 改善了大脑中的葡萄糖代谢并恢复了 ATP 生产水平。这些观察结果表明，PLD减轻了MPTP诱导的早期PD样症状，其作用机制可能与促进神经元葡萄糖代谢有关。