Apoptosis is one of the major mechanisms of neuronal injury during ischemic–reperfusion
(I/R). Mitochondrial division inhibitor (mdivi-1) is a selective inhibitor of mitochondrial
fission protein Drp1. The previous experiments support that mdivi-1 reduce I/R injury
in the heart model of rat, but the neuroprotective effect of the mdivi-1 is not yet
clearly defined at the cellular levels in brain. In our present study, we estimated
a brain model of I/R injury in vitro by subjecting oxygen and glucose deprivation
(OGD) followed by reoxygenation to the cultured rat primary hippocampal cells, which
aimed to find the neuroprotective mechanism of mdivi-1. The cell was pretreated with
mdivi-1 for 40 minutes and then ischemia for 6 hours followed by reperfusion for 20 hours.
The redox state, cell apoptosis, and expression of Drp1, Bcl-2, Bax, and cytochrome
C proteins were measured. The data showed that administration of mdivi-1 at the doses
of 50 μM significantly reduced oxidative stress, attenuated cell apoptosis, upregulated
Bcl-2 expression, and downregulated Drp1, Bax, and cytochrome C expression. The results
suggested that mdivi-1 protected brain from OGD reperfusion injury, which through
suppressing the ROS initiated mitochondrial pathway.
Key Words
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Article info
Publication history
Published online: April 28, 2014
Accepted:
December 16,
2013
Received in revised form:
December 10,
2013
Received:
November 14,
2013
Identification
DOI: https://doi.org/10.1016/j.jstrokecerebrovasdis.2013.12.021
Copyright
© 2014 National Stroke Association. Published by Elsevier Inc. All rights reserved.