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Hajipour H, Sedaghat K. Vitamin D Improves the Maternal Hypothyroidism-induced Cognitive Decline in the Rat Offspring. BCN 2026; 17 (1) :143-158
URL: http://bcn.iums.ac.ir/article-1-3412-fa.html

Introduction: Thyroid hormones (THs) are vital for fetal and neonatal nervous system development. Mild maternal hypothyroidism might render cognitive impairment in offspring during adulthood, by producing oxidative stress, inflammation, and lowering brain-derived neurotrophic factor (BDNF). Vitamin D has anti-oxidant and anti-inflammatory actions. Therefore, we investigated whether vitamin D administration during gestation in hypothyroid dams or after birth would improve cognitive function in offspring.
Methods: For this study, we used propylthiouracil (PTU) to induce hypothyroidism in pregnant rats from the sixth day of gestation until delivery. A group of pregnant rats received vitamin D (5 or 10 mg/kg) along with PTU, while another group received that after delivery until the weaning of offspring and continued for the offspring until they were sacrificed. At the 60th postnatal day, a novel object recognition (NOR) test was performed. Protein assays for lipid peroxidation, superoxide dismutase (SOD), interleukin-6 (1L-6:), tumor necrosis factor alpha (TNF-α), and BDNF were performed in the hippocampus and prefrontal cortex.
Results: Results indicated that maternal hypothyroidism reduced cognitive functions in the offspring, and that vitamin D administered during gestation improved memory decline and recognition of the novel object. Vitamin D, either during or after birth, markedly altered oxidative stress, inflammation, and BDNF levels in the brain.
Conclusion: This study indicates that maternal hypothyroidism-induced oxidation, inflammation, and decreased BDNF are passed and remain with the offspring into their adulthood, as possible causes of cognitive decline. Vitamin D administration, especially during pregnancy, may improve cognitive function by modulating the underlying mechanisms.