Vitamin D treatment ameliorates memory function through downregulation of BAX and upregulation of SOD2 mRNA expression in transient global brain ischaemic injury in rats.

Introduction: Ischaemic stroke induces oxidative stress with SOD2 downregulation, and BAX upregulation producing apoptosis. Vitamin D is a fat-soluble hormone that has a neuroprotective effect. The aim of this study is to elucidate the role of vitamin D in memory function, oxidative stress and apoptosis in transient global brain schaemic injury (TGBII) model.

Materials and methods: TGBII was performed in male Wistar rats (3 to 5 months, 150 to 300 g) which underwent bilateral common carotid artery occlusion (BCCAO) for 20 minutes, then reperfused for 10 days (BCCAO group, n = 6). Two groups of BCCAO were treated with intraperitoneal injection of calcitriol 0.125 μg/kgBW (VD1 group) and 0.5 μg/kgBW (VD2 group). The spatial memory function was tested using a probe test with Morris water maze (MWM). mRNA expression of BAX and SOD2 were assessed by the RT-PCR method. Meanwhile, immunohistochemical staining was used for identification of SOD2 protein. Statistical analysis is tested using one-way ANOVA followed by post-hoc LSD.

Results: MWM showed a shorter duration in target quadrant of BCCAO group than the SO group, which is associated with BAX upregulation and SOD2 downregulation. The VDtreated groups had longer duration probe test compared to BCCAO. Furthermore, VD-treated groups had a longer duration in probe test with lower mRNA expression of BAX and higher expression of SOD2. However, there was no significant difference in VD1 and VD2. Immunostaining showed a reduced SOD2 signal in pyramidal cell of CA1 area in BCCAO group and ameliorated in VD1 and VD2 groups.

Conclusion: Vitamin D ameliorates memory function and attenuates oxidative stress and apoptosis in the TGBII model.