LAUSR

Neuron damage contributes to ischemic brain injury. Although FMS-like tyrosine kinase-3 (FLT3) plays a critical role in neuron survival, its function and molecular mechanism in cerebral ischemia/reperfusion injury is unclear. In the present study, we exposed SH-SY5Y cells to oxygen and glucose deprivation/reoxygenation (OGD/R) to mimic ischemia/reperfusion injury. We found that FLT3 and MAPK14/p38α expression increased in OGD/R-treated cells. FLT3 silence significantly increased OGD/R-induced SH-SY5Y cell survival, inhibited reactive oxygen species production. Also, we observed that FLT3 silence suppressed OGD/R-induced SH-SY5Y cell apoptosis, apoptosis related protein Bax level and caspase-3 activity was decreased and Bcl-2 expression was increased in FLT3 silence SH-SY5Y cell treated with OGD/R. Furthermore, FLT3 depletion induced MAPK14/p38α inhibition in SH-SY5Y cultures after OGD/R exposure. These findings suggest that MAPK14/p38α overexpression reverses the action of FLT3 silence in OGD/R-induced SH-SY5Y cells. They also provide the first evidence that FLT3 silence has a neuroprotective role in OGD/R-induced SH-SY5Y cell damage. These data provide insight about potential neuroprotective molecular for ischemia/reperfusion injury.