Abstract
To investigate the effects of the GluN2C subunit on cerebral ischemia-reperfusion injury, we fabricated magnetic nano-gene vectors to inhibit and overexpress GluN2C in rat hippocampal neurons. The present study comprised six experimental groups: normal control (Control); oxygen and glucose deprivation withreoxygenation (OGD/R); Glu2NC si-RNA knockdown (si-RNA); GluN2C si-RNA knockdown and oxygen-glucose deprivation with reoxygenation (si-RNA+OGD/R); GluN2C overexpression (GluN2C); and GluN2C overexpression and oxygen-glucose deprivation with reoxygenation (GluN2C+OGD/R). Cells were then cultured for 6 h, 12 h, and 24 h under standard conditions. GluN2C expression was detected by Western blotting. Cell activity was determined using MTT assays. Apoptosis was measured by flow cytometry. GluN2C protein levels in the GluN2C and GluN2C+OGD/R groups increased with reoxygenation time. GluN2C protein levels were significantly higher in the GluN2C group compared to the GluN2C+OGD/R group at all measured timepoints. No differences in GluN2C protein levels were observed between the other four experimental groups at any timepoint. After 6 h of reoxygenation, neuronal activity in the si-RNA+OGD/R group was significantly higher than in the GluN2C+OGD/R group (0.451±0.006 vs. 0.419±0.005; P <0.05). Compared to the OGD/R group, neuronal activity was higher in the si-RNA+OGD/R group and lower in the GluN2C+OGD/R group after 12 h and 24 h of reoxygenation. Neuronal activity was significantly higher in the si-RNA+OGD/R group compared to the GluN2C+OGD/R group. Compared to the OGD/R group, the rate of neuronal apoptosis was lower in the si-RNA+OGD/R group and higher in the GluN2C+OGD/R group increased. The rate of neuronal apoptosis rate was significantly lower in the si-RNA+OGD/R group compared to the GluN2C+OGD/R group at 6 h, 12 h, and 24 h after reoxygenation. The findings of the present study demonstrate the role of the GluN2C subunit in nerve injury during cerebral ischemia-reperfusion injury.
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