DL-2-amino-3-phosphonopropionic acid protects primary neurons from oxygen-glucose deprivation induced injury

Cerebral infarction is a type of ischemic stroke and is one of the main causes of irreversible brain damage. Although multiple neuroprotective agents have been investigated recently, the potential of DL-2-amino-3-phosphonopropionic acid (DL-AP(3)) in treating oxygen-glucose deprivation (OGD)-induced neuronal injury, has not been clarified yet. This study was aimed to explore the role of DL-AP(3) in primary neuronal cell cultures. Primary neurons were divided into four groups: (1) A control group that was not treated; (2) DL-AP3 group treated with 10 mu M of DL-AP3; (3) OGD group, in which neurons were cultured under OGD conditions; (4) OGD + DL-AP(3) group, in which OGD model was first established and then the cells were treated with 10 mu M of DL-AP(3). Neuronal viability and apoptosis were measured using Cell Counting Kit-8 and flow cytometry. Expressions of phospho-Akt1 (p-Akt1) and cytochrome C were detected using Western blot. The results showed that DL-AP(3) did not affect neuronal viability and apoptosis in DL-AP(3) group, nor it changed p-Akt1 and cytochrome C expression (p > 0.05). In OGD + DL-AP(3) group, DL-AP(3) significantly attenuated the inhibitory effects of OGD on neuronal viability (p < 0.001) and reduced OGD induced apoptosis (p < 0.01). In addition, the down-regulation of p-Akt1 and up-regulation of cytochrome C, induced by OGD, were recovered to some extent after DL-AP(3) treatment (p < 0.05 or p < 0.001). Overall, DL-AP(3) could protect primary neurons from OGD-induced injury by affecting the viability and apoptosis of neurons, and by regulating the expressions of p-Akt1 and cytochrome C.