Ginkgolide B protects hippocampal neurons from apoptosis induced by beta-amyloid 25-35 partly via up-regulation of brain-derived neurotrophic factor.

Alzheimer's disease is a complex genetic disease in the global prevalence of up to 15 million people. The accumulation of beta-amyloid peptides leads to the subsequent disruption of neuronal process, abnormal phosphorylation of tau and ultimately the dysfunction and death of neurons. Ginkgolide B is a well-defined plant extract which is safe in nature, effective, economic and has minor side effects. This study aims at investigating the neuroprotective effects of Ginkgolide B against Aβ25-35-induced apoptosis in cultured hippocampal neurons, and further exploring the possible mechanisms concerned. We first conducted the study of the Aβ25-35-induced apoptosis characterized by the changes in cell viability, morphology, extracellular K(+) concentration, lactate dehydrogenase level, and the caspase-3 activity in hippocampal neurons. Moreover, the expression of brain-derived neurotrophic factor mRNA and the protein synthesis in neurons were detected via RT-PCR and Western-blot assay. It was found out that Aβ25-35-induced apoptosis was attenuated by Ginkgolide B. Ginkgolide B caused brain-derived neurotrophic factor up-regulation when cells were subjected to Aβ25-35 insults. The above results indicate that Ginkgolide B may significantly dampen Aβ25-35-induced apoptosis, and the neuroprotective effects may be intimately associated with brain-derived neurotrophic factor up-regulation caused by Ginkgolide B. These findings may demonstrate the neuroprotective effects of Ginkgolide B and offer new evidences to the possible mechanisms.