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Ginkgolides shield towards amyloid-beta1-42-mediated synapse injury in vitro.


Mol Neurodegener. 2008 Jan 7 ;3:1. Epub 2008 Jan 7. PMID: 18179689

Summary Title: 

Ginkgolides shield towards amyloid-beta1-42-mediated synapse injury in vitro.


BACKGROUND: The early phases of Alzheimer’s illness (AD) are carefully related to the manufacturing of the Abeta1-42 peptide, lack of synapses and gradual cognitive decline. Since some epidemiological research confirmed that EGb 761, an extract from the leaves of the Ginkgo biloba tree, had a useful impact on delicate types of AD, the consequences of a few of the main elements of the EGb 761 extract (ginkgolides A and B, myricetin and quercetin) on synapse injury in response to Abeta1-42 have been examined.RESULTS: The addition of Abeta1-42 to cortical or hippocampal neurons diminished the quantities of cell related synaptophysin, a pre-synaptic membrane protein that’s important for neurotransmission, indicating synapse injury. The results of Abeta1-42 on synapses have been obvious at concentrations roughly 100 fold lower than that required to kill neurons; the synaptophysin content material of neuronal cultures was diminished by 50% by 50 nM Abeta1-42. Pre-treatment of cortical or hippocampal neuronal cultures with ginkgolides A or B, however not with myrecitin or quercetin, protected towards Abeta1-42-induced lack of synaptophysin. This protecting impact was achieved with nanomolar concentrations of ginkgolides. Earlier research indicated that the ginkgolides are platelet-activating issue (PAF) receptor antagonists and right here we present that Abeta1-42-induced lack of synaptophysin from neuronal cultures was additionally diminished by pre-treatment with different PAF antagonists (Hexa-PAF and CV6209). PAF, however not lyso-PAF, mimicked the consequences Abeta1-42 and triggered a dose-dependent discount within the synaptophysin content material of neurons. This impact of PAF was vastly diminished by pre-treatment with ginkgolide B. In distinction, ginkgolide B didn’t have an effect on the lack of synaptophysin in neurons incubated with prostaglandin E2.CONCLUSION: Pre-treatment with ginkgolides A or B protects neurons towards Abeta1-42-induced synapse injury. These ginkgolides additionally diminished the consequences of PAF, however not these of prostaglandin E2, on the synaptophysin content material of neuronal cultures, outcomes in step with prior stories that ginkgolides act as PAF receptor antagonists. Such observations recommend that the ginkgolides are lively elements of Ginkgo biloba preparations and will shield towards the synapse injury and the cognitive loss seen through the early phases of AD.

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