• Neuroscience letters · Oct 2016

    Post-ischemia mdivi-1 treatment protects against ischemia/reperfusion-induced brain injury in a rat model.

    • Xuesong Ma, Yuying Xie, Yifan Chen, Baoqing Han, Jun Li, and Sihua Qi.
    • Department of Anesthesiology, Fourth Affiliated Hospital, Harbin Medical University, 37 Yiyuan Street, Nangang District, Harbin 150001, China; School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China.
    • Neurosci. Lett. 2016 Oct 6; 632: 23-32.

    AbstractWhen given prior to brain ischemia, mitochondrial division inhibitor-1 (mdivi-1) attenuates the brain damage caused by ischemia. Here, we investigated the potential effects of post-ischemia mdivi-1 treatment (1mg/kg, i.p., administered immediately after 2h of ischemia and prior to reperfusion) using a MCAO rat model. Mdivi-1 treatment decreased infarct volume and improved neurological function. In addition, cytochrome C release was attenuated, and neuronal apoptosis was decreased. The mitochondrial fission protein dynamin-related protein 1 (Drp1) was decreased in the mitochondrial fraction but increased in the cytosolic fraction. Mdivi-1 treatment augmented the increases in the mRNA expression of peroxisome proliferator-activated receptor coactivator-1α, nuclear respiratory factor-1, and mitochondrial transcriptional factor A. In conclusion, when given after ischemia and prior to reperfusion, mdivi-1 can protect against brain damage by inhibiting the mitochondria-mediated apoptosis induced by mitochondrial fission. Post-ischemia mdivi-1 treatment might promote I/R-induced mitochondrial biogenesis. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

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