The present study aimed to investigate betanin’s neuroprotective effect in mice with rotenone-induced Parkinson-like motor dysfunction and neurodegeneration. Forty male ICR mice were divided into 4 groups: Sham-veh, Rot-veh, Rot-Bet100 and Rot-Bet200. Rotenone at 2.5 mg/kg/48 h was subcutaneous injected in Rot groups, and betanin at 100 and 200 mg/kg/48 h were given alternately with the rotenone injections in Bet groups for 6 weeks. Motor dysfunctions were evaluated weekly using hanging wire and rotarod tests. Brain oxidative status including malondialdehyde, reduced glutathione, catalase, superoxide dismutase, with neuronal degeneration in the motor cortex, striatum and substantia nigra par compacta were evaluated. The immunohistochemical densities of tyrosine hydroxylase in striatum and in substantia nigra par compacta were also measured. We found that rotenone significantly decreased the time to fall in a hanging wire test after the 4^th week and after the rotarod test at the 6^th week (p < 0.05). The percentage of neuronal degeneration in substantia nigra par compacta, striatum and motor cortex significantly increased (p < 0.05), and the tyrosine hydroxylase density in substantia nigra par compacta and in striatum significantly decreased (p < 0.05). Betanin at 100 and 200 mg/kg significantly prevented substantia nigra par compacta, striatum and motor cortex neuronal degeneration (p < 0.05) and maintained tyrosine hydroxylase density in substantia nigra par compacta and in striatum (p < 0.05). These findings appeared concurrently with improved effects on the time to fall in hanging wire and rotarod tests (p < 0.05). Treatment with betanin significantly prevented increased malondialdehyde levels and boosted reduced glutathione, catalase and superoxide dismutase activities (p < 0.05). Betanin exhibits neuroprotective effects against rotenone-induced Parkinson in mice regarding both motor dysfunction and neurodegeneration. Betanin’s neurohealth benefit relates to its powerful antioxidative property. Therefore, betanin use in neurodegenerative disease is interesting to study.

本研究旨在研究甜菜碱对鱼藤酮诱导的帕金森样运动功能障碍和神经变性小鼠的神经保护作用。将 40 只雄性 ICR 小鼠分为 4 组：Sham-veh、Rot-veh、Rot-Bet100 和 Rot-Bet200。Rot组皮下注射2.5 mg/kg/48 h的鱼藤酮，Bet组皮下注射100和200 mg/kg/48 h的甜菜素，连续6周。每周使用吊线和旋转棒测试评估运动功能障碍。评估了脑氧化状态，包括丙二醛、还原型谷胱甘肽、过氧化氢酶、超氧化物歧化酶，以及运动皮层、纹状体和黑质致密部的神经元变性。还测量了纹状体和黑质致密部中酪氨酸羟化酶的免疫组织化学密度。^{第周和第 6周}的旋转棒测试后周（p < 0.05）。黑质致密部、纹状体和运动皮层神经元变性百分比显着增加（p < 0.05），黑质致密部和纹状体中酪氨酸羟化酶浓度显着降低（p < 0.05）。100 和 200 mg/kg 的甜菜素可显着预防黑质致密部、纹状体和运动皮层神经元变性 (p < 0.05)，并维持黑质致密部和纹状体中的酪氨酸羟化酶密度 (p < 0.05)。这些发现同时出现在吊线和转棒测试中对坠落时间的改善影响（p < 0.05）。甜菜碱处理可显着防止丙二醛水平升高，并增强还原型谷胱甘肽、过氧化氢酶和超氧化物歧化酶的活性（p < 0.05）。Betanin 在运动功能障碍和神经变性方面对小鼠鱼藤酮诱导的帕金森表现出神经保护作用。甜菜碱的神经健康益处与其强大的抗氧化特性有关。因此，在神经退行性疾病中使用甜菜碱是很有趣的研究。