Mitochondria play a key role in cell survival by perfoming functions such as adenosine
tri-phosphate (ATP) synthesis, regulation of apoptotic cell death, calcium storage. Hypoxic conditions
induce mitochondrial dysfunction, which leads to endothelial injury in cerebral ischemia.
Functional disorders include the following: collapse of mitochondrial membrane potential, reduction
of ATP synthesis, and generation of reactive oxygen species (ROS). Bendavia, a novel tetra-peptide,
has been reported to restrict the uncoupling of the mitochondrial membrane chain, protect the synthesis
of ATP, and inhibit ROS generation. In the present study, we investigated whether bendavia
protects mitochondria under hypoxic and starved conditions by using human brain microvascular
endothelial cells (HBMVECs). After pre-treatment with bendavia, we exposed HBMVECs to oxygen
glucose deprivation (OGD) for 6 h. We then assessed cell viability, the level of caspase-3/7 activity,
ROS generation, mitochondrial membrane potential, ATP contents, and the number of mitochondria.
Bendavia recovered cell viability and reduced the caspase-3/7 activity induced by OGDinduced
damage. Bendavia also recovered mitochondrial functions. These results suggest that bendavia
protects mitochondrial function against OGD-induced injury and inhibits apoptosis in
HBMVECs. Consequently, our findings indicate that bendavia might become the new therapeutic
drug of choice to target mitochondria in case of cerebral ischemia.