Table 1.

Effects of vitamin D in experimental stroke models—in vitro studies.

Model	Cell Treatment	Effects of Vitamin D	Reference
Glu and NMDA-induced excitotoxic damage in rat primary hippocampal neurons	1,25(OH)2D3 (0.1–1000 nM) NMDA (100 μM), Glu (5 μM)	1,25(OH)2D3 (1–100 nM) ↑cell viability ↓VGCC	[95]
Glu and dopaminergic toxins-induced rat mesencephalic cells damage	1,25(OH)2D3 (1–100 nM) Glu (1 mM) H2O2 (30 μM) Calcium ionophore (A23187, 1 μM) MPP+ (30 μM) 6-OHDA (100 μM)	↑cell viability ↓ROS	[96]
Glu-induced damage in primary rat cortical neurons	1,25(OH)2D3 (10–100 nM)/3–9 DIV Glu (100 μM)	↑cell viability ↑VDR mRNA ↑MAP-2 ↑GAP-43 ↑synapsin-1	[97]
Primary neocortical, hippocampal and cerebellar cell cultures exposed to Glu	1,25(OH)2D3 (50 and 100 nM)/30 min, 1, 3, 6 or 9 h after Glu (1 mM)	↓excitotoxicity ↓caspase-3 activity	[98]
Glu-induced primary cortical neurons damage	Progesterone (0.1-80 μM) and 1,25(OH)2D3 (1–100 nM) individually or in different combinations Glu (0.5 μM)	↓neuronal loss ↑p-ERK1/2	[99]
OGD model in primary cortical neurons	Progesterone (0.1–80 μM) and 1,25(OH)2D3 (0.001–5 μM) individually or in different combinations during OGD and reoxygenation	↓neuronal loss	[100]
Hypoxia model in C57BL/6J mice primary neuronal cells	cholecalciferol, 0.01–1 µM/14DIV, 20 min before hypoxia, during hypoxia and immediately after reoxygenation	cholecalciferol-1 µM ↓cell viability, ↓the neuron-glial functional structure cholecalciferol-0.01-0.1 µM ↑cell viability ↑the functional structure and activity of neuron–glial networks	[101]

↑: increase; ↓: decrease; 1,25(OH)2D3: calcitriol; DIV: days in vitro; ERK1/2: extracellular signal-regulated kinase 1 and 2; GAP-43: growth-associated protein-43; Glu: glutamate; L-VGCC: voltage-dependent calcium channels; MAP-2: microtubule-associated protein-2; MPP+: 1-Methyl-4-phenylpyridinium; OGD: oxygen glucose deprivation; 6-OHDA: 6-hydroxydopamine; ROS: reactive oxygen species; VDR: vitamin D receptor.