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甜菜碱对鱼藤酮诱导的帕金森病小鼠的益处。

Benefits of betanin in rotenone-induced Parkinson mice.

机构信息

Animal Toxicology and Physiology Specialty Research Unit (ATPSRU), Physiology Division, Department of Zoology, Faculty of Science, Kasetsart University, 50 Ngamwongwan road, Jatuchak, Bangkok, 10900, Thailand.

出版信息

Metab Brain Dis. 2021 Dec;36(8):2567-2577. doi: 10.1007/s11011-021-00826-0. Epub 2021 Aug 26.

Abstract

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 week and after the rotarod test at the 6 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.

摘要

本研究旨在探讨甜菜红素对鱼藤酮诱导的帕金森样运动功能障碍和神经退行性变小鼠的神经保护作用。将 40 只雄性 ICR 小鼠分为 4 组:假手术-载体、鱼藤酮-载体、鱼藤酮-甜菜红素 100 和鱼藤酮-甜菜红素 200。鱼藤酮以 2.5mg/kg/48h 皮下注射于鱼藤酮组,甜菜红素以 100 和 200mg/kg/48h 交替注射于鱼藤酮组,持续 6 周。每周使用悬挂线和旋转棒试验评估运动功能障碍。评估大脑氧化状态,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酪氨酸羟化酶的免疫组织化学密度。结果发现,鱼藤酮显著降低了悬挂线试验第 4 周和旋转棒试验第 6 周的跌倒时间(p<0.05)。黑质致密部、纹状体和运动皮层的神经元变性百分比显著增加(p<0.05),黑质致密部和纹状体的酪氨酸羟化酶密度显著降低(p<0.05)。甜菜红素 100 和 200mg/kg 显著预防黑质致密部、纹状体和运动皮层神经元变性(p<0.05),维持黑质致密部和纹状体的酪氨酸羟化酶密度(p<0.05)。这些发现与悬挂线和旋转棒试验跌倒时间的改善效果同时出现(p<0.05)。甜菜红素治疗显著降低了丙二醛水平,提高了还原型谷胱甘肽、过氧化氢酶和超氧化物歧化酶的活性(p<0.05)。甜菜红素对鱼藤酮诱导的小鼠帕金森具有神经保护作用,可改善运动功能障碍和神经退行性变。甜菜红素的神经健康益处与其强大的抗氧化特性有关。因此,甜菜红素在神经退行性疾病中的应用值得研究。

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