In neurodegenerative diseases, progressive oxidative stress is a major event that precedes neuronal death. Oxidative stress is characterized by an imbalance between oxidants and antioxidants. This imbalance induced oxidative molecular and cell damage, reducing cellular viability. 3-Nitropropionic acid (3NP) causes oxidative stress and other molecular and cellular changes similar to those observed in neurons of patients with Huntington’s disease. Since carvedilol and melatonin act as free-radical scavengers, this study examined the effect of carvedilol (10⁻⁵ M) and melatonin (10⁻⁵ M) on oxidative and cell damage induced by 3NP in N1E-115 neuroblastoma cells. Carvedilol and melatonin prevented the increases in lipid peroxidation and total LDH activity, as well as the depletion of reduced glutathione (GSH) and the reduction of antioxidative enzymes activities in N1E-115 cells incubated with 100 mM 3NP. All these carvedilol and melatonin effects were more intense when the drugs were added before rather than after inducing the damage by 3NP. These results also provided evidence supporting the hypothesis that carvedilol and melatonin can be useful for treating neurodegenerative diseases, such as Huntington’s disease.

中文翻译：

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卡维地洛和褪黑激素对神经母细胞瘤中 3-硝基丙酸诱导的神经毒性的神经保护作用。

在神经退行性疾病中，进行性氧化应激是神经元死亡之前的主要事件。氧化应激的特点是氧化剂和抗氧化剂之间的不平衡。这种不平衡导致氧化分子和细胞损伤，降低细胞活力。3-硝基丙酸 (3NP) 会导致氧化应激和其他分子和细胞变化，类似于在亨廷顿病患者的神经元中观察到的变化。由于卡维地洛和褪黑激素作为自由基清除剂，本研究检查了卡维地洛 (10 ^-5 M) 和褪黑激素 (10 ^-5M) 在 N1E-115 神经母细胞瘤细胞中由 3NP 诱导的氧化和细胞损伤。卡维地洛和褪黑激素可防止脂质过氧化和总 LDH 活性的增加，以及还原型谷胱甘肽 (GSH) 的消耗和与 100 mM 3NP 孵育的 N1E-115 细胞中抗氧化酶活性的降低。所有这些卡维地洛和褪黑激素的作用在诱导 3NP 损伤之前而不是在诱导损伤之前添加药物时更强烈。这些结果还提供了支持卡维地洛和褪黑激素可用于治疗神经退行性疾病（如亨廷顿病）的假设的证据。