Vitamin D ameliorates memory function in association with reducing senescence and upregulating neurotrophin mRNA expression in transient global cerebral ischemic injury model in rats.

Introduction: Ischaemic stroke induces oxidative stress, mitochondrial damage, inflammation and senescence and the decrease of cognitive function. Vitamin D is a fat-soluble vitamin that has a neuroprotective effect to repair the function of the nervous system. The aim of this study is to investigate the effect of vitamin D on memory function, p16, p21 (senescence), and nerve growth factor (NGF) mRNA expression on the hippocampus after transient global cerebral ischemic.

Materials and methods: The study was designed as quasiexperimental with a control group that only received posttests. We performed in vivo study with an induction bilateral common carotid artery occlusion (BCCAO) model and vitamin D injection for 10 days. A total of 24 rats were divided into four groups (n = 6): Sham operation (SO [control]), BCCAO (transient global cerebral ischemic model not given vitamin D), VD1 (BCCAO + vitamin D 0.125 μg/kgBW), and VD2 (BCCAO + vitamin D 0.5 μg/kgBW). The spatial memory function was tested with the Morris water maze. We performed immunohistochemistry to localise p16 expression. p16, p21 and NGF mRNA expression were assessed by reverse transcriptase (RT-PCR) method.

Results: The vitamin D treatment group required shorter mileage to find the platform and probe test. The total time spent was longer in the target quadrant than in non-target. The Vitamin D-treated group had lower p16 and p21 mRNA expression and higher NGF mRNA expression than the BCCAO group. Immunostaining showed p16 signal in the pyramidal cell of CA1 area in the BCCAO group.

Conclusion: Vitamin D repairs memory function, senescence expression was lower and NGF was higher in the BCCAO model.