The Study On The Expression Of BDNF By Akt/eNOS Pathways In Early Brain Damage In Rats After SAH

Objective: Detection the expression of the brain-derived neurotropicfactor (BDNF) in early brain injury (EBI) after subarachnoid hemorrhage(SAH), explore its promotion of endothelial cell regeneration mechanismsand pathways to provide a new method for the treatment of patients withSAH.Methods: Randomly divide72healthy male SD rats into shamoperation group and after SAH12h,24h,48h group,18in each group.Select the preoptic pool blood injection method to establish the rat modelof SAH. The expression levels of BNDF, VEGF and eNOs in thehippocampus were examined at12,24and48h following SAH usingWestern Blot and RT-PCR, and measured brain water content in rats.Results: The expression of BNDF, VEGF and eNOs increaseddramatically at12h，reached the peak at24h，and started to decline at48h following SAH, but still maintained a high level. They were positivelycorrelated in each other’s rBV=0.973，P=0.014；rNV=0.964，P=0.021；rBN=0.948，P=0.016. The contents of brain water increased progressively at 12h，reached the maximum level at24h and maintained a high lebel at48h following SAH. The protein expression levels of BDNF and the contentsof brain water were positively correlated r=0.947，P=0.023.Conclusion: BDNF played a very important role in the pathologicalprocess of cerebral ischemia and hypoxia after SAH, and is likely toincrease expression of VEGF by regulating PI3K/Akt/eNOS channels.