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Nogo-A antibody treatment enhances neuron recovery after sciatic nerve transection in rats.

Authors :
ZHANG, Z.-W.
JIANG, J.-J.
LUAN, M.-C.
MA, Z.-J.
GAO, F.
YU, S.-J.
Source :
European Review for Medical & Pharmacological Sciences; Apr2017, Vol. 21 Issue 8, p1780-1786, 7p
Publication Year :
2017

Abstract

OBJECTIVE: The use of an antibody to block the neurite outgrowth inhibitor Nogo-A has been of great interest for promoting axonal recovery as a treatment for peripheral nerve injuries. The present study aimed to investigate the signaling pathway of p75 neurotrophin receptor (NTR) and Nogo receptor (NgR) in a sciatic nerve transection (SNT) rat model and evaluate the underlining mechanisms. MATERIALS AND METHODS: Seventy-five Sprague-Dawley (SD) rats were randomly divided into 3 groups (n=25), namely the sham group, sciatic nerve transection (model) group and No-go-A-pAb group. Following euthanasia, spinal cord and sciatic nerve of the operation site were harvested, fixed in formalin. Hematoxylin and eosin (HE) staining was used to evaluate the sciatic nerve pathology. The mRNA and protein expression levels of Nogo-A, NTR were assessed by Real-time polymerase chain reaction (RT-PCR) and Western blotting, respectively. RESULTS: Histology showed enhanced regeneration of spinal axon in the anti-Nogo-A anti-body group. At 48 hours after operation, mRNA of Nogo-A and NTR were higher in model group compared with control group. mRNAs were at their highest levels at 1 week, while these were at normal levels after 4 weeks in Nogo-A-pAb group. The protein levels of Nogo-A and NTR were higher in model group compared with sham-operation group at 1-week after operation; Nogo-A-pAb could reduce these proteins levels. CONCLUSIONS: The results suggested No-go-A antibody might represent a promising repair strategy to promote recovery following SNT. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
11283602
Volume :
21
Issue :
8
Database :
Supplemental Index
Journal :
European Review for Medical & Pharmacological Sciences
Publication Type :
Academic Journal
Accession number :
122741383