Objective   To investigate the molecular mechanism of vascular endothelial growth factor (VEGF) for early brain injury after subarachnoid hemorrhage (SAH).    Methods   A total of 90 male Sprague-Dawley rats were randomly divided into 3 groups

control group (n=30)

sham operation group (n=30)

and SAH group (n=30). SAH model was established by endovascular perforation without opening cranium

and then neurological score was determined. At different time points (12

24

and 48 h) after operation

the tissues of hippocampus CA1 area were sampled. The histopathological changes of cerebral tissue were observed by HE staining

and ultrastructural changes by electron microscopy. The expression of VEGF were determined by immunohistochemical staining and Western blot analysis. The apoptosis of nerve cell were detected by TUNEL.     Results   In SAH group

the neurological function scores were significantly lower (P0.05). The axons and capillaries in SAH group were obviously damaged

the living neurons were much lesser than in sham group

the VEGF level was significantly enhanced (P0.05)

and a lot of apoptosis cells were observed and their number reached a peak at 48 h (P0.05). The expression of VEGF was positively correlated with the TUNEL positive cells after SAH (r=0.847

P0.01).    Conclusion   VEGF contributes to early brain injury

and the increased expression of VEGF in hippocampal CA1 may induce neuronal apoptosis following SAH.