BACKGROUND

Primary cells have the same heterogeneity and differentiation capacity that has potential as an ischemic stroke models. It is hoped that primary cells from non-human primates that have genetic similarities to humans can provide molecular information and become more accurate data for use in drug screening, especially stroke therapy. B27 is a supplement commonly used in neuronal cell cultures, but there are concerns that its effects will interfere with the neuroprotective processes of the drug candidates being tested.

AIM

This research will prove the demonstration of neurons as an ischemic stroke model and the effects of B27 in (Mf) neurons as a model for ischemic stroke under oxygen glucose deprivation (OGD).

METHODS

Neurons were obtained from a collection of biological materials collected during previous research. Neuronal validation was performed using immunocytochemistry with the marker β-tubulin. Expression of the apoptotic response was performed by real time- polymerase chain reaction/(RT-PCR) using Bax, BCL-2, caspase-9, and p53 gene markers. Characterization of neurons in terms of positive tβubulin markers and induction of OGD in neurons can be performed for 6 h to model ischemic stroke.

RESULTS

This study showed that cultured neurons under OGD conditions can experience apoptosis, namely by increasing pro-apoptosis and decreasing anti-apoptosis. However, B27 supplementation increased the expression of anti-apoptotic Bcl-2 genes and decreased proapoptotic genes such as Bax, caspase 9, and p53.

CONCLUSION

Neuron culture from Mf can be used as an model of ischemic stroke, and B27 supplementation in neurons exerts neuroprotective effects on the induction of OGD.