Abstract: Objective To investigate the effect of recombinant rat vascular endothelial growth factor 165 (rrVEGF165) on serum endostatin variations and brain derived neurotrophic factor (BDNF) with its tyrosin-kinase B（TrkB）receptor mRNA expression in spinal cord tissues. Methods Forty-eight rats were randomly divided into three groups: the sham-operation group(S), the model group(M) and the treatment group of rrVEGF165(V). The spinal cord ischemia-reperfusion lesion models were established by using Naslund abdominal aorta occlusion and declamped 90 minutes later. Histopathological changes in the spinal cord were observed by hematoxylin and eosion (HE) staining. Serum endostatin and BDNF levels were determined by enzyme linked immunosorbent assay (ELISA). Expressions of TrkB receptor mRNA were determined by reversetransferent polymerase chain reaction (RTPCR). ResultsInconvertible spinal damage was model group, histopathological changes in the spinal cord of group V were remarkably improved. For serum endostatin(ES): in group M, the level of endostatin began to increase after 6h post-reperfusion and remained till day 7. In group V, ES was increased at 6?h after reperfusion but that was not maintained in the following days. Serum BDNF and expression of TrkB mRNA: in group M, serum BDNF was decreased at 6?h, then returned to the control level at day 2, but was decreased more severely at day 7 which was only about 59.1% of the control level and was significant lower than that at 6h(P＜0.05). The expression of mRNA of spinal cord TrkB receptor was up-regulated at 6?h, returned to the control level at day 2, and then kept down-regulating to the lowest level at day 7 after reperfusion. In group V, in contrast, serum BDNF was significantly increased at 6?h, then returned back to the control group at day 7, and the expression of TrkB mRNA maintained a sustainable upregulation level. ConclusionSpinal rrVEGF165 administration can alleviate the increase of ES and the decrease of serum BDNF induced by spinal cord ischemic reperfusion injury, and enhances the up-regulation of mRNA expression of TrkB receptor.

Key words: Spinal cord ischemiareperfusion, Recombinant rat vascular endothelial growth factor 165, Endostatin, Brain derived neurotrophic factor, Tyrosinkinase B receptor, Rat, Wistar