RESEARCH ARTICLE |
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Year : 2012 | Volume
: 44
| Issue : 4 | Page : 480-484 |
Vasoactive agent buflomedil up-regulated expression of vascular endothelial growth factor in a rat model of sciatic nerve crush injury
Jin-Rong Tang1, Le Wu2, Jian-Hua Su1, Ping Zhang3, Long-Bin Yu4, Hang Xiao2
1 Department of Neurology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China 2 Department of Neurotoxicology, Nanjing Medical University, Nanjing, China 3 Department of Pathology, the Second Affiliated Hospital of Nanjing Medical University-210018, Nanjing, China 4 Department of Statistics, Nanjing Medical University, Nanjing, China
Correspondence Address:
Hang Xiao Department of Neurotoxicology, Nanjing Medical University, Nanjing China
 Source of Support: Medical Research Council [grant number: Natural science of Jiangsu province BK2001116]., Conflict of Interest: None  | Check |
DOI: 10.4103/0253-7613.99312
Objectives: To study the effect of Buflomedil on the morphological repair on crush injury of sciatic nerve and also the expression of vascular endothelial growth factor (VEGF).
Materials and Methods: Rat sciatic nerves were crushed by pincers. All of the 400 Sprague Dawley rats were randomly divided into: Sham-operated; saline; saline + VEGF-antibody; Buflomedil; and Buflomedil + VEGF antibody groups. The expression of VEGF in dorsal root ganglia (DRGs), following crush injury to sciatic nerves, was studied by RT-PCR, immunohistochemistry. The effects of Buflomedil on expression of VEGF and repair of neural pathology were also evaluated.
Results: VEGF mRNA was significantly increased in Buflomedil and Buflomedil + VEGF-antibody groups, compared with other groups. The number of VEGF-positive neurons was significantly increased in the Buflomedil and the saline groups. Besides, Buflomedil also caused less pathological changes in DRGs.
Conclusions: The vasoactive agent Buflomedil may decrease the pathological lesion and improve the functional rehabilitation of peripheral nerves, which may correlate to upregulation of the expression of VEGF, following crush injury to the peripheral nerves.
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