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Abstract
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-AP3) in treating oxygen-glucose deprivation (OGD)-induced neuronal injury, has not been clarified yet. This study was aimed to explore the role of DL-AP3 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 μM of DL-AP3; (3) OGD group, in which neurons were cultured under OGD conditions; and (4) OGD + DL-AP3 group, in which OGD model was first established and then the cells were treated with 10 μM of DL-AP3. 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-AP3 did not affect neuronal viability and apoptosis in DL-AP3 group, nor it changed p-Akt1 and cytochrome c expression (p > 0.05). In OGD + DL-AP3 group, DL-AP3 significantly attenuated the inhibitory effects of OGD on neuronal viability (p < 0.001), and reduced OGD induced apoptosis (p < 0.01). Additionally, the down-regulation of p-Akt1 and up-regulation of cytochrome c, induced by OGD, were recovered to some extent after DL-AP3 treatment (p < 0.05 or p < 0.001). Overall, DL-AP3 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.
Highlights
Cerebral infarction is a type of ischemic stroke and is one of the main causes of irreversible brain damage [1]
Primary neurons were divided into four groups: (1) A control group that was not treated; (2) DL-AP3 group treated with 10 μM of DL-AP3 for 6 hours; (3) oxygen-glucose deprivation (OGD) group, in which neurons were cultured under OGD conditions for 12 hours; (4) OGD + DL-AP3 group, in which OGD model was first established and the cells were treated with 10 μM of DL-AP3 for 6 hours [17]
DL-AP3 significantly attenuated the inhibitory effect of OGD on neuronal viability (p < 0.001), in OGD + DL-AP3 group
Summary
Cerebral infarction is a type of ischemic stroke and is one of the main causes of irreversible brain damage [1]. Risk factors of cerebral infarction include high blood pressure, diabetes mellitus, tobacco smoking, obesity, and dyslipidemia [2]. Excitatory amino acids (EAAs) have been identified to play a role in causing irreversible ischemic brain damage [6]. An increasing number of studies has demonstrated a vital role of glutamate in a focal ischemic model of the human brain [7,8]. Ke et al have found that MK-801 may alleviate ischemia/reperfusion injury of rat sciatic nerve by inhibiting the activation of tumor necrosis factor-α [13]. Adachi et al found that phencyclidine-induced the decrease of synaptic connectivity by inhibiting the secretion of brain-derived neurotrophic factor in cultured cortical neurons [14]
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