Brain-derived neurotrophic factor in ischemic preconditioning neuroprotective role model.docVIP

Brain-derived neurotrophic factor in ischemic preconditioning neuroprotective role model.doc

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 PAGE \* MERGEFORMAT 11 Brain-derived neurotrophic factor in ischemic preconditioning neuroprotective role model [Abstract] Objective To study the brain-derived neurotrophic factor (BDNF) in the pre-ischemia model in the expression and role in ischemic tolerance in the formation of the molecular signaling mechanism. SD rats were prepared by four-vessel occlusion model of the brain and pre- ischemia model, Western blot, immunoprecipitation and other techniques to detect the expression of BDNF in each experimental group, and its receptor tyrosine kinase receptor B (TrkB) and downstream extracellular signal-regulated protein kinase (ERK1 / 2) phosphorylation level. Results The expression of BDNF pre-ischemic group, TrkB and ERK1 / 2 phosphorylation compared with ischemia / reperfusion significantly elevated (P lt;0.05), and TrkB receptor antagonist K252a can reduce the elevated activation levels (P lt;0.05). Conclusions Ischemic preconditioning activates BDNF-TrkB-ERK1 / 2 signaling pathway to achieve its neuroprotective effect. [Keywords:] brain-derived neurotrophic factor; pre-ischemia; ischemic tolerance Abstract: Objective To investigate the expression level and the role of brain-derived neurotrophic factor (BDNF) in ischemic preconditioning (IP) model and the underlying molecular signaling mechanism of ischemic tolerance. Methods Ischemic preconditioning model was induced by the four-vessel occlusion in Sprague-Dawley rats. Immunoblotting and immunoprecipitation methods were employed to determine the variations in the expression level of BDNF, the phosphorylation levels of its receptor, tyrosine kinase receptor B (TrkB) and the downstream extracellular-signal-regulated kinase (ERK1 / 2) . Results In the IP group, the levels of BDNF expression and TrkB and ERK1 / 2 phosphorylation increased (P lt;0.05), as compared to the Ischemia / Reperfusion group, while the pretreatment with K252a, a TrkB receptor antagonist, reversed the preconditioning- induced

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