Abstract
ObjectiveThe objective of this study is to establish a co-culture model of mouse neurons and microglial cells, and to analyze the mechanism of action of oxygen glucose deprivation (OGD) and transient oxygen glucose deprivation (tOGD) preconditioning cell models.ResultsMouse primary neurons and BV2 microglial cells were successfully cultured, and the OGD and tOGD models were also established. In the co-culture of mouse primary neurons and microglial cells, the cell number of tOGD mouse neurons and microglial cells was larger than the OGD cell number, observed by a microscope. CCK-8 assay result showed that at 1h after treatment, the OD value in the control group is lower compared to all the other three groups (P < 0.05). The treatment group exhibited the highest OD value among the four groups. The results observed at 5h were consistent with the results at 1 h. Flow cytometry results showed that at 1h after treatment the apoptosis percentages is higher in the control group compared to other three groups (P < 0.05).Materials and MethodsMouse brain tissues were collected and primary neurons cells were cultured. In the meantime mouse BV2 microglia cells were cultured. Two types of cells were co-cultured, and OGD and tOGD cell models were established. There were four groups in the experiment: control group (OGD), treatment group (tOGD+OGD), placebo group (tOGD+OGD+saline) and minocycline intervention group (tOGD+OGD+minocycline). CCK-8 kit was used to detect cell viability and flow cytometry was used to detect apoptosis.ConclusionsIn this study, mouse primary neurons and microglial cells were co-cultured. The OGD and tOGD models were established successfully. tOGD was able to effectively protect neurons and microglial cells from damage, and inhibit the apoptosis caused by oxygen glucose deprivation.
Highlights
Ischemic stroke, a common clinical disease known as cerebral infarction, is most likely caused by various reasons and exhibits blockage of cerebral circulation supply, cerebral ischemia and hypoxia, leading to necrosis, as well as the subsequent neuronal functional damage [1]
In the co-culture of mouse primary neurons and microglial cells, the cell number of transient oxygen glucose deprivation (tOGD) mouse neurons and microglial cells was larger than the Oxygen and glucose deprivation (OGD) cell number, observed by a microscope
The OGD and tOGD models were established successfully. tOGD was able to effectively protect neurons and microglial cells from damage, and inhibit the apoptosis caused by oxygen glucose deprivation
Summary
A common clinical disease known as cerebral infarction, is most likely caused by various reasons and exhibits blockage of cerebral circulation supply, cerebral ischemia and hypoxia, leading to necrosis, as well as the subsequent neuronal functional damage [1]. Cerebral infarction is one of the main causes of death in clinical practice, with poor prognosis and causing a heavy burden of disease [2]. It has become a hot research topic to search an effective therapy for ischemic stroke. At present a number of studies have utilized OGD in vitro models to investigate an effective treatment method for ischemic stroke and have shown good results [9, 10]. Oxygen and glucose deprivation preconditioning refers to the tolerability of tissue to oxygen and glucose deprivation damage, acquired by www.impactjournals.com/oncotarget once or multiple times of transient oxygen and glucose deprivation [11,12,13]
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