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month download article/chapter seizure-induced oxidative stress cerebral ischemia/reperfusion injury pilocarpine-induced epileptic rats drp1-activated mitochondrial fission early brain injury cell death induced subarachnoid hemorrhage research full article pdf traumatic brain injury diminishing cell death harbin medical university dynamin-related protein 1 privacy choices/manage cookies improved sod activity related subjects mitochondrial fission protein natural science foundation inhibiting oxidative stress experimental subarachnoid hemorrhage standard intravascular perforation anti-apoptotic pathway pilocarpine-induced seizures regulating mitochondrial fission mitochondrial division inhibitor mitochondrial division inhibitor-1 blood–brain barrier alleviated brain edema hippocampal neurons aneurysmal subarachnoid hemorrhage cassidy-stone brain injuries mechanism endoplasmic reticulum stress inhibits mitochondrial fragmentation article wu check access instant access cell death european economic area mdivi-1 reduced levels hd striatal susceptibility improving functional outcome dysfunctional endothelial cells inhibits caspase-3 activation temporal lobe epilepsy loma linda university altered mitochondrial dynamics mitochondrial calcium uniporter conditions privacy policy bergmann-leitner es

Questions {❓}

• Rosdah AA, J KH, Delbridge LM, Dusting GJ, Lim SY (2016) Mitochondrial fission - a drug target for cytoprotection or cytodestruction?

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         headline:Mdivi-1 Alleviates Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats, Possibly via Inhibition of Drp1-Activated Mitochondrial Fission and Oxidative Stress
         description:Mdivi-1 is a selective inhibitor of mitochondrial fission protein, Drp1, and can penetrate the blood–brain barrier. Previous studies have shown that Mdivi-1 improves neurological outcomes after ischemia, seizures and trauma but it remains unclear whether Mdivi-1 can attenuate early brain injury after subarachnoid hemorrhage (SAH). We thus investigated the therapeutic effect of Mdivi-1 on early brain injury following SAH. Rats were randomly divided into four groups: sham; SAH; SAH + vehicle; and SAH + Mdivi-1. The SAH model was induced by standard intravascular perforation and all of the rats were subsequently sacrificed 24 h after SAH. Mdivi-1 (1.2 mg/kg) was administered to rats 30 min after SAH. We found that Mdivi-1 markedly improved neurologic deficits, alleviated brain edema and BBB permeability, and attenuated apoptotic cell death. Mdivi-1 also significantly reduced the expression of cleaved caspase-3, Drp1 and p-Drp1(Ser616), attenuated the release of Cytochrome C from mitochondria, inhibited excessive mitochondrial fission, and restored the ultra-structure of mitochondria. Furthermore, Mdivi-1 reduced levels of MDA, 3-NT, and 8-OHdG, and improved SOD activity. Taken together, our data suggest that Mdivi-1 exerts neuroprotective effects against cell death induced by SAH and the underlying mechanism may be inhibition of Drp1-activated mitochondrial fission and oxidative stress.
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      headline:Mdivi-1 Alleviates Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats, Possibly via Inhibition of Drp1-Activated Mitochondrial Fission and Oxidative Stress
      description:Mdivi-1 is a selective inhibitor of mitochondrial fission protein, Drp1, and can penetrate the blood–brain barrier. Previous studies have shown that Mdivi-1 improves neurological outcomes after ischemia, seizures and trauma but it remains unclear whether Mdivi-1 can attenuate early brain injury after subarachnoid hemorrhage (SAH). We thus investigated the therapeutic effect of Mdivi-1 on early brain injury following SAH. Rats were randomly divided into four groups: sham; SAH; SAH + vehicle; and SAH + Mdivi-1. The SAH model was induced by standard intravascular perforation and all of the rats were subsequently sacrificed 24 h after SAH. Mdivi-1 (1.2 mg/kg) was administered to rats 30 min after SAH. We found that Mdivi-1 markedly improved neurologic deficits, alleviated brain edema and BBB permeability, and attenuated apoptotic cell death. Mdivi-1 also significantly reduced the expression of cleaved caspase-3, Drp1 and p-Drp1(Ser616), attenuated the release of Cytochrome C from mitochondria, inhibited excessive mitochondrial fission, and restored the ultra-structure of mitochondria. Furthermore, Mdivi-1 reduced levels of MDA, 3-NT, and 8-OHdG, and improved SOD activity. Taken together, our data suggest that Mdivi-1 exerts neuroprotective effects against cell death induced by SAH and the underlying mechanism may be inhibition of Drp1-activated mitochondrial fission and oxidative stress.
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      name:Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Neurosurgery and Anesthesiology, Loma Linda University, Loma Linda, USA
      name:Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China
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