| Inflammation plays a vital role in the pathogenesis of ischemic stroke. Brain-derived neurotrophic factor (BDNF) may protect brain tissues against ischemic injury. The aim of this study was to investigate whether intranasal BDNF could exert neuroprotection against ischemic insult by modulating the local inflammation in rats with ischemic stroke. Rats were subjected to temporary occlusion of the right middle cerebral artery (120min) and intranasal BDNF or vehicle was carried on2h after reperfusion. Infarct volume and neuron injury were measured using triphenyltetrazolium chloride, Nissl staining and TUNEL assay, respectively. Microglia were detected by immunohistofluorescence using OX-42and ED1antibody. Tumor necrosis factor-a, interleukinlO and their mRNAs were evaluated by enzyme-linked immunosorbent assay and real-time quantitative polymerase chain reaction. DNA-binding activity of nuclear factor-kappa B was detected by electrophoretic mobility shift assay. BDNF level in brain tissues was markedly raised following intranasal administration. There were more Nissl positive and less TUNEL positive neurons in BDNF group than in control group while intranasal BDNF did not reduce the infarct volume significantly (n=6,0.27±0.04vs.0.24±0.05, P>0.05). BDNF increased the number of activated microglia (OX-42positive) and phagocytotic microglia (ED1positive). BDNF suppressed tumor necrosis factor-a and its mRNA expression while increasing the expression of interleukinlO and its mRNA. BDNF also increased DNA-binding activity of nuclear factor-kappa B (n=6,49.78±1.23vs.52.89±1.64, P<0.05). Our data suggested intranasal BDNF might protect the brain against ischemic insult by modulating local inflammation via regulation of the levels of cellular, cytokine and transcription factor in the experimental stroke. |
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