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Ginkgolide B preconditioning protects neurons towards ischaemia-induced apoptosis.


J Cell Mol Med. 2009 ;13(11-12):4474-83. PMID: 19602048

Summary Title: 

Ginkgolide B preconditioning protects neurons towards ischaemia-induced apoptosis.


Ischaemic preconditioning (IP) has been reported to guard the mind towards subsequent deadly ischaemia, however it has not been used clinically to forestall ischaemic harm due to security considerations. The purpose of the current research was to see whether or not Ginkgolide B (GB) is able to preconditioning as IP to guard neurons towards ischaemic harm; if that’s the case, which mechanism is concerned. Cultured mouse cortical neurons at day 8 had been pre-treated with GB (120 micromol/l) for twenty-four hrs or uncovered to short-term ischaemia (1 hr) adopted by 24-hr regular tradition to induce IP earlier than being handled with extreme ischaemia (5 hrs). GB and IP considerably elevated cell viability, expression of hypoxia-inducible factor-1 alpha (HIF-1alpha), erythropoietin (EPO), phosphorylated Dangerous at serine 136 (136p-Dangerous) and phosphorylated glycogen synthase kinase- 3beta at serine 9 (p-GSK-3beta), and decreased the proportion of apoptotic cells and the extent of lively caspase-3 in severely ischaemic neurons. Furthermore, LY294002 that could be a particular inhibitor of phosphatidylinositol 3-kinase (PI3K) considerably diminished the improved expression of HIF-1alpha, EPO and 136p-Dangerous induced by GB and IP. These outcomes recommend that GB, like IP in neurons, is able to preconditioning towards ischaemia-induced apoptosis, the mechanism of which can contain the PI3K signalling pathway.

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