Neuregulin1[beta] Effects on Brain Tissue via ERK5-Dependent MAPK Pathway in a Rat Model of Cerebral Ischemia-Reperfusion Injury

• Published in: Journal of molecular neuroscience Vol. 61; no. 4; p. 607
• Main Authors: Gu, Ning, Ge, Keli, Hao, Cui, Ji, Yaqing, Li, Hongyun, Guo, Yunliang
• Format: Journal Article
• Language: English
• Published: Totowa Springer Nature B.V 01.04.2017
• Subjects: Apoptosis; Carotid arteries; Doppler effect; Ischemia; Kinases; Proteins; Stroke; Transmission electron microscopy; Veins & arteries; China
• ISSN: 0895-8696; 1559-1166
• DOI: 10.1007/s12031-017-0902-4

Neuregulin1[beta] (NRG1[beta]), a member of the excitomotor of tyrosine kinase receptor (erbB) family, was recently shown to play a neuroprotective role in cerebral ischemia-reperfusion injury. The present study analyzed the effects and its possible signaling pathway of NRG1[beta] on brain tissues after cerebral ischemia-reperfusion injury. A focal cerebral ischemic model was established by inserting a monofilament thread to achieve middle cerebral artery occlusion, followed by an NRG1[beta] injection via the internal carotid artery. NRG1[beta] injection resulted in significantly improved neurobehavioral activity according to the modified neurological severity score test. Tetrazolium chloridestaining revealed a smaller cerebral infarction volume; hematoxylin-eosin staining and transmission electron microscopy showed significantly alleviated neurodegeneration in the middle cerebral artery occlusion rats. Moreover, expression of phosphorylated MEK5, phosphorylated ERK5, and phosphorylated MEK2C increased after NRG1[beta] treatment, and the neuroprotective effect of NRG1[beta] was attenuated by an injection of the MEK5 inhibitor, BIX02189. Results from the present study demonstrate that NRG1[beta] provides neuroprotection following cerebral ischemia-reperfusion injury via the ERK5-dependent MAPK pathway.