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Objective: To explore the regulating mechanism of neureglin1β on ERK5 signaling pathway in rats with cerebral ischemia reperfusion injury.Methods: A focal cerebral ischemic model was established by inserting a monofilament thread into the middle cerebral artery occlusion (MCAO).In accordance with the principle of randomized, controlled with the sham operation group, the model group, the treatment group, the inhibitor group, the inhibitor plus treatment group.The internal carotid artery injection 5μl (2 μg/kg) NRG13 intervention treatment.The neurobehavioral functions were evaluated with the modified neurological severity score (mNSS) test.The cerebral infarct volumes were measured with triphenyl tetrazolium chloride (TTC) staining.The morphology of cortical brain tissues were observed with hematoxylin-eosin staining.The apoptotic cells were counted with terminal deoxynucleotidyl transferase dUTP nick-end labeling, and the expressions of pMEK5, pERK, pMEF2C were determined by immunohistochemical assay and Western blot.Results: After cerebral ischemia reperfusion injury, the rats appeared neurobehavioral dysfunction and cerebral infarction in cortex, the nerve cell damage is aggravated and the apoptotic cells increased, the expressions of pMEK5, pERK5, pMEF2C compensatory enhanced.Compared with model group, the expressions of pMEK5, pERK5, pMEF2C further enhanced,apoptotic cells decreased significantly, alleviate the damage of nerve cells, cerebral infarction volume shrinking, neurobehavioral functions improved in the treatment group.In inhibitor group, the nerve cell damage is serious, apoptotic cells increased, and the expressions of pMEK5, pERK5, pMEF2C decreased significantly.Inhibitor plus treatment group rats, pMEK5, pERK5, pMEF2C expressed obviously higher than those inhibitor group, the nerve cell damage and apoptosis cells reduced significantly than those in the inhibitor group.Conclusion: The results suggested that NRG1β could play a neuroprotective role by activating the MEK5-ERK5-MEF2C signaling pathway to inhibit neuronal apoptosis and inflammation induced by cerebral ischemia reperfusion injury in rats.