The present study aimed to evaluate the effect of folic acid treatment in an animal model of aging induced by D-galactose (D-gal). For this propose, adult male Wistar rats received D-gal intraperitoneally (100 mg/kg) and/or folic acid orally (5 mg/kg, 10 mg/kg or 50 mg/kg) for 8 weeks. D-gal caused habituation memory impairment, and folic acid (10 mg/kg and 50 mg/kg) reversed this effect. However, folic acid 50 mg/kg per se caused habituation memory impairment. D-gal increased the lipid peroxidation and oxidative damage to proteins in the prefrontal cortex and hippocampus from rats. Folic acid (5 mg/kg, 10 mg/kg, or 50 mg/kg) partially reversed the oxidative damage to lipids in the hippocampus, but not in the prefrontal cortex, and reversed protein oxidative damage in the prefrontal cortex and hippocampus. D-gal induced synaptophysin and BCL-2 decrease in the hippocampus and phosphorylated tau increase in the prefrontal cortex. Folic acid was able to reverse these D-gal-related alterations in the protein content. The present study shows folic acid supplementation as an alternative during the aging to prevent cognitive impairment and brain alterations that can cause neurodegenerative diseases. However, additional studies are necessary to elucidate the effect of folic acid in aging.

本研究旨在评估叶酸治疗在 D-半乳糖（D-gal）诱导衰老动物模型中的效果。为此，成年雄性 Wistar 大鼠腹腔注射 D-gal（100 mg/kg）和/或口服叶酸（5 mg/kg、10 mg/kg 或 50 mg/kg），持续 8 周。 D-gal 会导致习惯性记忆障碍，而叶酸（10 毫克/千克和 50 毫克/千克）可逆转这种影响。然而，叶酸50mg/kg本身会导致习惯性记忆障碍。 D-gal 增加了大鼠前额皮质和海马的脂质过氧化和蛋白质氧化损伤。叶酸（5毫克/千克、10毫克/千克或50毫克/千克）部分逆转了海马中脂质的氧化损伤，但不能逆转前额皮质的氧化损伤，并逆转了前额皮质和海马中蛋白质的氧化损伤。 D-gal 诱导海马突触素和 BCL-2 减少，以及前额皮质磷酸化 tau 蛋白增加。叶酸能够逆转这些与 D-gal 相关的蛋白质含量变化。目前的研究表明，叶酸补充剂可以作为衰老过程中的替代方案，以预防认知障碍和可能导致神经退行性疾病的大脑改变。然而，还需要更多的研究来阐明叶酸在衰老中的作用。