Journal of integrative neuroscience · 2025
Vitamin D3 Treatment Reduces Epileptic Neuronal Damage by Inhibiting Apoptosis and Increasing Vitamin D Receptor Expression in an In Vivo Epileptic Model.
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Nie Yin-Yue, Huang Lu-Yue, Wang Lu-Chuan, Zeng Pei, Gong Chao, Song Lin, Guo Jin, Zhou Shaobo
Аннотация
BACKGROUND: Vitamin D (VitD) deficiency is prevalent in more than half of patients treated with antiepileptic drugs. The number of seizures decreases by more than 40% after vitamin D3 supplementation. This study aimed to investigate the antiepileptic effects of vitamin D3 by using an in vivo epileptic model.
METHOD: Sprague-Dawley rats received pentylenetetrazole (i.p.) treatment to induce epilepsy and were then treated with sodium valproate, VitD, or a combination of VitD and paricalcitol.
RESULTS: Vitamin D3 treatment improved epileptic behavior, as evidenced by increased latency time and a significant reduction in epileptic scores on the seventh day after pentylenetetrazole challenge. Improvements in cell morphology and reduced neuronal damage were observed as well as decreased apoptosis rates caused by epilepsy. Although no significant changes in the calcium-sensing receptor (CaSR) were observed in any group, the level of VitD receptor (VDR) significantly increased in groups treated with vitamin D3 alone, and with paricalcitol and sodium valproate.
CONCLUSIONS: The study demonstrated the effect of vitamin D3 on reducing neuronal damage caused by epilepsy. The neuroprotective effects of vitamin D3 treatment may be attributed to the inhibition of cell apoptosis and the increase in the expression of VitD receptors induced by epilepsy.
METHOD: Sprague-Dawley rats received pentylenetetrazole (i.p.) treatment to induce epilepsy and were then treated with sodium valproate, VitD, or a combination of VitD and paricalcitol.
RESULTS: Vitamin D3 treatment improved epileptic behavior, as evidenced by increased latency time and a significant reduction in epileptic scores on the seventh day after pentylenetetrazole challenge. Improvements in cell morphology and reduced neuronal damage were observed as well as decreased apoptosis rates caused by epilepsy. Although no significant changes in the calcium-sensing receptor (CaSR) were observed in any group, the level of VitD receptor (VDR) significantly increased in groups treated with vitamin D3 alone, and with paricalcitol and sodium valproate.
CONCLUSIONS: The study demonstrated the effect of vitamin D3 on reducing neuronal damage caused by epilepsy. The neuroprotective effects of vitamin D3 treatment may be attributed to the inhibition of cell apoptosis and the increase in the expression of VitD receptors induced by epilepsy.