Exogenous brain-derived neurotrophic factor attenuates neuronal apoptosis and neurological deficits after subarachnoid hemorrhage in rats.

Brain-derived neurotrophic factor (BDNF) is a growth factor crucial for neuronal survival, while its role in subarachnoid hemorrhage (SAH)-induced neuronal apoptosis remains unclear. The aim of the present study was to investigate whether administering exogenous BDNF can protect against neuronal apoptosis and neurological deficits following SAH in a rat model. The BDNF level was found to be significantly decreased in the basal cortex at 6, 12, 24, 48 and 72 h following SAH. Exogenous BDNF significantly decreased the expression of Bax and reduced activation of caspase-3 and caspase-9 and the number of apoptotic neurons. Moreover, exogenous BDNF treatment significantly improved the neurological deficits at 72 h and long-term behavioral deficits (day 14) following SAH in a rat model. These findings indicate that exogenous BDNF attenuated SAH-induced neuronal injury in rats.
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