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ApoE mimetic ameliorates motor deficit and tissue damage in rat spinal cord injury.
Abstract
Apolipoprotein E (apoE), a plasma protein responsible for transporting lipid and cholesterol,
modulates responses of the central nervous system to injury. Small peptides derived
from the receptor-binding region of apoE can simulate some important bioactivities
of apoE holoprotein and offer neuroprotection against brain injury. We tested whether
COG1410, an apoE-mimetic peptide, provides protection in a rat model of spinal cord
injury (SCI). Traumatic injury was created at T8 by a cortical impact device. Injured
rats were randomized to four treatment groups: vehicle, 0.15, 0.3, or 0.6 mg/kg COG1410;
sham surgery rats received vehicle. Basso, Beattie, Bresnahan neurological score was
evaluated prior to injury and at 1, 3, 7, and 14 days after injury. Histological changes
were evaluated at 14 days. All injured rats lost body weight during the first week
following injury. Body weight recovery was significantly improved in rats treated
with COG1410. Mechanical impact resulted in severe motor deficit, and most animals
had a BBB score of 0-1 at 24 hours postinjury. COG1410-treated rats showed significantly
improved functional recovery and ameliorated motor deficit at 14 days postinjury.
Histological analysis showed that COG1410 groups had a significantly reduced lesion
size at the site of injury, a larger preserved luxol fast blue-stained area, and more
visible neurons in the surrounding area of injury. Microglial activation was also
significantly suppressed. These findings indicate that this apoE mimetic effectively
improved neurological and histological outcome following SCI in rats, and the effect
was associated with inhibition of microglial activation.
Type
Journal articleSubject
MicrogliaNeurons
Animals
Rats
Rats, Wistar
Movement Disorders
Spinal Cord Injuries
Disease Models, Animal
Body Weight
Apolipoproteins E
Neurologic Examination
Recovery of Function
Cell Death
Dose-Response Relationship, Drug
Male
Leukoencephalopathies
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https://hdl.handle.net/10161/23278Published Version (Please cite this version)
10.1002/jnr.23371Publication Info
Wang, Ruihua; Hong, Jun; Lu, Miaomiao; Neil, Jessica E; Vitek, Michael P; Liu, Xiaozhi;
... Sheng, Huaxin (2014). ApoE mimetic ameliorates motor deficit and tissue damage in rat spinal cord injury.
Journal of neuroscience research, 92(7). pp. 884-892. 10.1002/jnr.23371. Retrieved from https://hdl.handle.net/10161/23278.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Huaxin Sheng
Associate Professor in Anesthesiology
We have successfully developed various rodent models of brain and spinal cord injuries
in our lab, such as focal cerebral ischemia, global cerebral ischemia, head trauma,
subarachnoid hemorrhage, intracerebral hemorrhage, spinal cord ischemia and compression
injury. We also established cardiac arrest and hemorrhagic shock models for studying
multiple organ dysfunction. Our current studies focus on two projects. One is to
examine the efficacy of catalytic antioxidant in treating cerebral is
Michael P. Vitek
Adjunct Associate Professor in Neurology
The overall interest of my laboratory is to identify the underlying causes of neurodegenerative
diseases such as Alzheimer's disease. Once causes or experimental endpoints are determined,
then strategies to find chemicals which can ameliorate pathophysiological events can
be devised. In general, we are working to create transgenic animals and validate them
as models of human disease. Our specific approach has been to study the function
of apolipoprotein-E (apoE) which Roses and coll
David Samuel Warner
Distinguished Distinguished Professor of Anesthesiology, in the School of Medicine
Humans may sustain a variety of forms of acute central nervous system injury including
ischemia, trauma, vasospasm, and perinatal hypoxemia. The Multidisciplinary Neuroprotection
Laboratories is dedicated to examining the pathophysiology of acute brain and spinal
cord injury with particular reference to disease states managed in the perioperative
or neurointensive care environments. Rodent recovery models of cerebral ischemia,
traumatic brain injury, cardiopulmonary bypass, subarachnoid he
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