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| 1,25(OH)2D3 deficiency may be associated with affective disorders, Parkinson's disease, Alzheimer's disease and cognitive abilities. To explore the protective effects of 1,25(OH)2D3 against glutamate-induced damage in a mouse-derived hippocampal HT-22 cells and underlying potential mechanism. The cell survival rate was determined with Cell Counting Kit-8. Cell cycle, apoptosis and reactive oxidative species (ROS) release were detected by FACs technology. Results showed that pretreatment 1,25(OH)2D3 effectively increase HT-22 cell viability up on glutamate exposure. This might be associated with the fact that 1,25(OH)2D3 significantly reduced the percentage of G0/G1 circles (G0/G1%) (p<0.01)，increased the proportion of S phase (S%) and G2/M phase (G2/M%) cells (p<0.01). Moreover, apoptosis in HT-22 cells showed the late cell apoptosis rate was decreased (p<0.05) in glutamate group incubated with 1,25(OH)2D3 (i.e. combination group) compared with the glutamate only group. There was an inverse association between the concentration of 1,25(OH)2D3 and apoptosis rate. Meanwhile, the ROS release was elevated in the combination group (p<0.05). Our study indicates that 1,25(OH)2D3 might adversely affect glutamate-induced apoptosis in the HT-22 cells，this might be owing to the fact that 1,25(OH)2D3 could increase cell proliferation and decrease late apoptosis rate. 1,25(OH)2D3 might be a promising therapeutic agent for the treatment of depression. |
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| Keywords:1, 25-dihydroxyvitamin D3; Glutamate; HT-22 cells; Neurotoxicity |
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