内分泌学
内科学
维生素
神经发生
维生素D与神经学
海马体
医学
线粒体生物发生
生物
线粒体
生物化学
神经科学
作者
Daria Korewo-Labelle,Mateusz Jakub Karnia,D. Myślińska,Jan Jacek Kaczor
标识
DOI:10.3390/ijms241813941
摘要
Dexamethasone (DEXA) is a commonly used steroid drug with immunosuppressive and analgesic properties. Unfortunately, long-term exposure to DEXA severely impairs brain function. This study aimed to investigate the effects of vitamin D3 supplementation during chronic DEXA treatment on neurogenesis, mitochondrial energy metabolism, protein levels involved in the BDNF-mediated Akt activity, and specific receptors in the hippocampus. We found reduced serum concentrations of 25-hydroxyvitamin D3 (25(OH)D3), downregulated proBDNF and pAkt, dysregulated glucocorticosteroid and mineralocorticoid receptors, impaired mitochondrial biogenesis, and dysfunctional mitochondria energy metabolism in the DEXA-treated group. In contrast, supplementation with vitamin D3 restored the 25(OH)D3 concentration to a value close to that of the control group. There was an elevation in neurotrophic factor protein level, along with augmented activity of pAkt and increased citrate synthase activity in the hippocampus after vitamin D3 administration in long-term DEXA-treated rats. Our findings demonstrate that vitamin D3 supplementation plays a protective role in the hippocampus and partially mitigates the deleterious effects of long-term DEXA administration. The association between serum 25(OH)D3 concentration and BDNF level in the hippocampus indicates the importance of applying vitamin D3 supplementation to prevent and treat pathological conditions.
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