Betanin, a natural food colorant with powerful antioxidative properties, has not been studied in terms of neurodegenerative disease intervention. Therefore, the present study aimed to investigate the neuroprotective effects of betanin against trimethyltin chloride (TMT) -induced neurodegeneration in mice. Forty male ICR mice were randomly divided into four groups: Sham-veh, TMT-veh, TMT-Bet50 and TMT-Bet100. In the TMT groups, neurodegeneration was induced with a one-time intraperitoneal injection of 2.6 mg/kg TMT. Betanin-treated groups (Bet) were given oral doses of 50 or 100 mg/kg dissolved in normal saline solution. Administrations were started 24 h prior to TMT injection and continued for 2 weeks. Anxious behavior and spatial cognition were evaluated, respectively. After behavioral tests, brain oxidative status, hippocampal histology and choline acetyltransferase (ChAT) activity were evaluated. Results showed that TMT significant induce anxious behavior and spatial learning and memory deficits (p < 0.05). These were found concurrently with significant decreases in CA1 ChAT activity, brain tissue catalase (CAT) and superoxide dismutase (SOD) activities with significant increase in hippocampal CA1 degeneration (p < 0.05). Betanin 100 mg/kg exhibited significant anxiolytic effect, preventive effect on CA1 degeneration and CA1 ChAT activity alteration as well as improvement of spatial learning and memory deficits (p < 0.05). These were found concurrently with significant increases of reduced glutathione, CAT and SOD activities as well as the decrease in malondialdehyde (p < 0.05). We conclude that betanin 100 mg/kg exhibits neuroprotective effects against TMT-induced neurodegeneration in mice via its anti-oxidative properties, protective against hippocampal CA1 degeneration and ChAT activity alteration. Therefore, betanin is interesting in further neurodegenerative therapeutic study and applications.

甜菜碱是一种具有强大抗氧化特性的天然食用色素，尚未在神经退行性疾病干预方面进行研究。因此，本研究旨在研究甜菜碱对三甲基氯化锡 (TMT) 诱导的小鼠神经变性的神经保护作用。40 只雄性 ICR 小鼠随机分为四组：Sham-veh、TMT-veh、TMT-Bet50 和 TMT-Bet100。在 TMT 组中，通过一次性腹腔注射 2.6 mg/kg TMT 诱导神经变性。甜菜碱治疗组 (Bet) 口服 50 或 100 毫克/千克溶解在生理盐水中的剂量。在 TMT 注射前 24 小时开始给药并持续 2 周。分别评估焦虑行为和空间认知。经过行为测试，大脑氧化状态，评估了海马组织学和胆碱乙酰转移酶 (ChAT) 活性。结果表明，TMT显着诱发焦虑行为和空间学习记忆缺陷。p  < 0.05)。这些与 CA1 ChAT 活性、脑组织过氧化氢酶 (CAT) 和超氧化物歧化酶 (SOD) 活性的显着降低同时发现，海马 CA1 变性显着增加 ( p  < 0.05)。Betanin 100 mg/kg 表现出显着的抗焦虑作用，对 CA1 变性和 CA1 ChAT 活性改变的预防作用以及空间学习和记忆缺陷的改善 ( p  < 0.05)。这些发现与还原型谷胱甘肽、CAT 和 SOD 活性的显着增加以及丙二醛的减少同时发生（p < 0.05)。我们得出结论，甜菜碱 100 mg/kg 通过其抗氧化特性、对海马 CA1 变性和 ChAT 活性改变的保护作用，对小鼠 TMT 诱导的神经变性具有神经保护作用。因此，甜菜碱在进一步的神经退行性治疗研究和应用中很有趣。