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Summary   Aims   DJ ‐1 is a key redox‐reactive neuroprotective protein implicated in regulation of oxidative stress after stroke. However, the molecular mechanism, especially the role of mitochondrial function, by which  DJ ‐1 protects neural cells in stroke remains to be elucidated. The aim of this study was to reveal whether  DJ ‐1 translocates into the mitochondria in exerting neuroprotection against oxidative stress. In particular, we examined  DJ ‐1 secretion from primary rat neural cells ( PRNC s) exposed to experimental stroke.    Methods  Primary rat neural cells were exposed to the oxygen–glucose deprivation ( OGD ), an established  in vitro  stroke model, and  DJ ‐1 translocation was measured by immunocytochemistry, and its secretion detected by  ELISA .    Results  Under  OGD ,  DJ ‐1 translocated into the healthy mitochondria, and significant levels of  DJ ‐1 protein were detected. Treatment with anti‐ DJ ‐1 antibody reduced cell viability and mitochondrial activity, and increased glutathione level. Interestingly,  OGD  reversed the ratio of astrocyte/neuron cells (6/4 to 4/6).    Conclusions  Altogether, these results revealed that  DJ ‐1 participates in the acute endogenous neuroprotection after stroke via the mitochondrial pathway. That  DJ ‐1 was detected immediately after stroke and efficiently translocated into the mitochondria offer a new venue for developing neuroprotective and/or neurorestorative strategies against ischemic stroke.

Oxygen–Glucose‐Deprived Rat Primary Neural Cells Exhibit DJ ‐1 Translocation into Healthy Mitochondria: A Potent Stroke Therapeutic Target