Abstract
Changes in expression of neurorepair and neuroregenerative factors were examined after transient cerebral ischemia in relation to the effects of tissue plasminogen activator (tPA) and the free radical scavenger edaravone. Physiological saline or edaravone was injected twice during 90 min of transient middle cerebral artery occlusion (tMCAO) in rats, followed by the same saline or tPA at reperfusion. Sizes of the infarct and protein factors relating to neurorepair and neuroregeneration were examined at 4 d after tMCAO. The protein factors examined were: a chondroitin sulfate proteoglycan neurocan, semaphorin type 3A (Sema3A), a myelin-associated glycoprotein receptor (Nogo receptor, Nogo-R), a synaptic regenerative factor (growth associated protein-43, GAP43), and a chemotropic factor netrin receptor (deleted in colorectal cancer, DCC). Two groups treated by edaravone only or edaravone plus tPA showed a reduction in infarct volume compared to the two groups treated by vehicle only or vehicle plus tPA. Immunohistochemistry and western blot analyses indicated that protein expression of neurocan, Sema3A, Nogo-R, GAP43, and DCC was decreased with tPA, but recovered with edaravone. Additive edaravone prevented the reductions of these five proteins induced by tPA. The present study demonstrates for the first time that exogenous tPA reduced protein factors involved in inhibiting and promoting axonal growth, but that edaravone ameliorated such damage in brain repair after acute ischemia.
| Original language | English |
|---|---|
| Pages (from-to) | 168-177 |
| Number of pages | 10 |
| Journal | Brain Research |
| Volume | 1436 |
| DOIs | |
| Publication status | Published - Feb 3 2012 |
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Keywords
- Acute ischemia
- Axonal growth
- Edaravone
- Neuroregeneration
- Neurorepair
- Tissue plasminogen activator
ASJC Scopus subject areas
- Neuroscience(all)
- Clinical Neurology
- Developmental Biology
- Molecular Biology
Cite this
Modifying neurorepair and neuroregenerative factors with tPA and edaravone after transient middle cerebral artery occlusion in rat brain. / Deguchi, Kentaro; Miyazaki, Kazunori; Tian, Fengfeng; Liu, Ning; Liu, Wentao; Kawai, Hiromi; Omote, Yosiho; Kono, Syoichiro; Yunoki, Taijun; Deguchi, Shoko; Abe, Koji.
In: Brain Research, Vol. 1436, 03.02.2012, p. 168-177.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Modifying neurorepair and neuroregenerative factors with tPA and edaravone after transient middle cerebral artery occlusion in rat brain
AU - Deguchi, Kentaro
AU - Miyazaki, Kazunori
AU - Tian, Fengfeng
AU - Liu, Ning
AU - Liu, Wentao
AU - Kawai, Hiromi
AU - Omote, Yosiho
AU - Kono, Syoichiro
AU - Yunoki, Taijun
AU - Deguchi, Shoko
AU - Abe, Koji
PY - 2012/2/3
Y1 - 2012/2/3
N2 - Changes in expression of neurorepair and neuroregenerative factors were examined after transient cerebral ischemia in relation to the effects of tissue plasminogen activator (tPA) and the free radical scavenger edaravone. Physiological saline or edaravone was injected twice during 90 min of transient middle cerebral artery occlusion (tMCAO) in rats, followed by the same saline or tPA at reperfusion. Sizes of the infarct and protein factors relating to neurorepair and neuroregeneration were examined at 4 d after tMCAO. The protein factors examined were: a chondroitin sulfate proteoglycan neurocan, semaphorin type 3A (Sema3A), a myelin-associated glycoprotein receptor (Nogo receptor, Nogo-R), a synaptic regenerative factor (growth associated protein-43, GAP43), and a chemotropic factor netrin receptor (deleted in colorectal cancer, DCC). Two groups treated by edaravone only or edaravone plus tPA showed a reduction in infarct volume compared to the two groups treated by vehicle only or vehicle plus tPA. Immunohistochemistry and western blot analyses indicated that protein expression of neurocan, Sema3A, Nogo-R, GAP43, and DCC was decreased with tPA, but recovered with edaravone. Additive edaravone prevented the reductions of these five proteins induced by tPA. The present study demonstrates for the first time that exogenous tPA reduced protein factors involved in inhibiting and promoting axonal growth, but that edaravone ameliorated such damage in brain repair after acute ischemia.
AB - Changes in expression of neurorepair and neuroregenerative factors were examined after transient cerebral ischemia in relation to the effects of tissue plasminogen activator (tPA) and the free radical scavenger edaravone. Physiological saline or edaravone was injected twice during 90 min of transient middle cerebral artery occlusion (tMCAO) in rats, followed by the same saline or tPA at reperfusion. Sizes of the infarct and protein factors relating to neurorepair and neuroregeneration were examined at 4 d after tMCAO. The protein factors examined were: a chondroitin sulfate proteoglycan neurocan, semaphorin type 3A (Sema3A), a myelin-associated glycoprotein receptor (Nogo receptor, Nogo-R), a synaptic regenerative factor (growth associated protein-43, GAP43), and a chemotropic factor netrin receptor (deleted in colorectal cancer, DCC). Two groups treated by edaravone only or edaravone plus tPA showed a reduction in infarct volume compared to the two groups treated by vehicle only or vehicle plus tPA. Immunohistochemistry and western blot analyses indicated that protein expression of neurocan, Sema3A, Nogo-R, GAP43, and DCC was decreased with tPA, but recovered with edaravone. Additive edaravone prevented the reductions of these five proteins induced by tPA. The present study demonstrates for the first time that exogenous tPA reduced protein factors involved in inhibiting and promoting axonal growth, but that edaravone ameliorated such damage in brain repair after acute ischemia.
KW - Acute ischemia
KW - Axonal growth
KW - Edaravone
KW - Neuroregeneration
KW - Neurorepair
KW - Tissue plasminogen activator
UR - http://www.scopus.com/inward/record.url?scp=84856004974&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84856004974&partnerID=8YFLogxK
U2 - 10.1016/j.brainres.2011.12.016
DO - 10.1016/j.brainres.2011.12.016
M3 - Article
C2 - 22221736
AN - SCOPUS:84856004974
VL - 1436
SP - 168
EP - 177
JO - Brain Research
JF - Brain Research
SN - 0006-8993
ER -