Abstract
The deficiency or supplementation of folic acid (FA) during the pregnancy can interfere in aging process. Therefore, the aim of the present study was to assess the impact of maternal deficiency and supplementation of AF on memory and neuroinflammation in the adult and old offspring of Wistar rats. Female and male Wistar rats were used for mating. After, the female rats pregnant remained for 28 days of pregnancy with different diets: AIN 93 diet or control, FA deficiency diet, AIN 93 diet + FA 5 mg/kg, AIN 93 diet + FA 10 mg/kg and AIN 93 diet + FA 50 mg/kg. The young adult (2-month-old) female offspring of all experimental groups and only the older (18-month-old) female offspring of rats with AIN 93 diet, FA deficiency diet and AIN 93 diet + AF 10mg/kg were subjected to open field habituation task and Y maze test and analyze of brain cytokine levels. The results show that the deficiency of FA and high supplementation (50 mg/kg) on the gestational period induced cognitive deficit in adult offspring. In the older, the control and FA deficiency group also showed damage. However, the FA 10 mg/kg group showed protection against this effect. It was observed that TNF-α and IL-β levels were increased in the hippocampus of 18-month-old offspring of control and FA deficiency group, and FA 10 mg/kg reversed this effect. The 2-month-old offspring of FA 50 mg/kg group showed reduction of IL-β level. Moreover, in the frontal cortex, it was observed that in adult offspring of FA 10 mg/kg group showed increase of IL-4 and FA 50 mg/kg induced reduction this cytokine. In the old animals was observed reduction of IL-4 level in the control group and increase in the FA 10 mg/kg group. In the hippocampus, the IL-4 levels of the adult offspring of FA deficiency and FA 50 mg/kg group were reduced. The adult offspring of FA 10 mg/kg group presented increase of IL-4 levels. Altogether, the results indicated that FA supplementation during pregnancy can protect the old offspring against the cognitive damage of aging, at least in part, by modulating inflammation.
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