Departamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, 88040-900 SC, Brazil.
J Mol Neurosci. 2013 Jan;49(1):68-79. doi: 10.1007/s12031-012-9892-4. Epub 2012 Oct 3.
Studies have demonstrated an association between stressful conditions and the onset of clinical depression. Considering the antidepressant-like properties of ascorbic acid in both experimental and clinical approaches, we evaluated the beneficial effect of this vitamin on restraint stress-induced behavioral and neurochemical alterations. Acute restraint stress caused a depressive-like behavior in the forced swimming test, accompanied by increased lipid peroxidation (cerebral cortex and hippocampus); increased superoxide dismutase (cerebral cortex and hippocampus), glutathione reductase (cerebral cortex), and glutathione peroxidase (cerebral cortex and hippocampus) activities; and elevated expression of Bcl-2 (hippocampus). Oral administration of ascorbic acid (1 mg/kg) or fluoxetine (10 mg/kg) 1 h before restraint stress prevented the stress-induced increase on immobility time in the forced swimming test. Moreover, this vitamin reduced lipid peroxidation to control levels and restored the activity of superoxide dismutase, glutathione reductase, and glutathione peroxidase. Ascorbic acid had no effect on the increased level of Bcl-2 induced by stress. Glutathione levels, glycogen synthase kinase-3β phosphorylation, and Bax expression were not altered by stress or ascorbic acid administration. Besides reinforcing the antioxidant potential of ascorbic acid, our results support the notion that oxidative stress plays a role in the pathogenesis and treatment of stress-induced depression.
研究表明，紧张的状况与临床抑郁症的发作之间存在关联。考虑到抗坏血酸在实验和临床方法中都具有抗抑郁特性，我们评估了这种维生素对束缚应激引起的行为和神经化学改变的有益影响。急性束缚应激会导致强迫游泳试验中出现类似抑郁的行为，同时伴随着脂质过氧化（大脑皮层和海马体）增加；超氧化物歧化酶（大脑皮层和海马体）、谷胱甘肽还原酶（大脑皮层）和谷胱甘肽过氧化物酶（大脑皮层和海马体）活性增加；Bcl-2（海马体）表达升高。束缚应激前 1 小时口服抗坏血酸（1mg/kg）或氟西汀（10mg/kg）可预防应激引起的强迫游泳试验中不动时间增加。此外，这种维生素可将脂质过氧化降低至对照水平，并恢复超氧化物歧化酶、谷胱甘肽还原酶和谷胱甘肽过氧化物酶的活性。抗坏血酸对应激引起的 Bcl-2 水平升高没有影响。应激或抗坏血酸给药均未改变谷胱甘肽水平、糖原合酶激酶-3β磷酸化和 Bax 表达。除了增强抗坏血酸的抗氧化潜力外，我们的结果还支持氧化应激在应激诱导的抑郁症发病机制和治疗中的作用的观点。
