2014•Shiyong yaowu yu linchuangRequires access

Hippocampal neurons protecting effect of propofol against hypoxia/reoxygenation via inducing the expression of nerve growth factor

Yan Feng

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Abstract

Objective To establish a model of hypoxia/re-oxygenation( H/R) injury to examine the neuroprotective effect of propofol,and explore the role of nerve growth factor( NGF) in this action. Methods Hippocampal neurons were randomly assigned to one of 7 groups: Control group( Con group); CoCl2 group; intralipid group( Intra group) : pretreated the neurons with 10% intralipid 90 μL,then added 300 μM CoCl2; propofol group: pretreated the neurons with 10,20,50,100 μM propofol for 1 h,then added 300 μM CoCl2,stimulated with no serum media 24 hours later. MTT method and FACS was used to detect the proliferation and apoptosis of neurons. Then RT-PCR method was used to showthe regulation of NGF and TrkA in propofol preconditioning H / R with different concentrations of propofol. To further investigate the effect of NGF / TrkA signaling pathway,the neurons were stimulated with 1. 0 μmol / LK252 a before treated with 50 μM propofol,expression of TrkA were measured by Western blot. Results H / R resulted in reduced cell viability and increased cell apoptosis in Hippocampal neurons,as indicated by MTT assay and FACS respectively( P 0. 01). Pretreatment with 50 μM propofol reversed H / R-induced neurotoxicity and induced a remarkable increase in NGF mRNA and TrkA mRNA expression and the inhibition of TrkA receptor by K252a( an inhibitor of Trk family members) altered the neuro-protective effect of propofol( P 0. 05 or 0. 01). Conclusion The findings suggest the potential effect of propofol for protecting hippocampal neuron against H / R through NGF / Trk signaling pathway partly.

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Objective To establish a model of hypoxia/re-oxygenation( H/R) injury to examine the neuroprotective effect of propofol,and explore the role of nerve growth factor( NGF) in this action. Methods Hippocampal neurons were randomly assigned to one of 7 groups: Control group( Con group); CoCl2 group; intralipid group( Intra group) : pretreated the neurons with 10% intralipid 90 μL,then added 300 μM CoCl2; propofol group: pretreated the neurons with 10,20,50,100 μM propofol for 1 h,then added 300 μM CoCl2,stimulated with no serum media 24 hours later. MTT method and FACS was used to detect the proliferation and apoptosis of neurons. Then RT-PCR method was used to showthe regulation of NGF and TrkA in propofol preconditioning H / R with different concentrations of propofol. To further investigate the effect of NGF / TrkA signaling pathway,the neurons were stimulated with 1. 0 μmol / LK252 a before treated with 50 μM propofol,expression of TrkA were measured by Western blot. Results H / R resulted in reduced cell viability and increased cell apoptosis in Hippocampal neurons,as indicated by MTT assay and FACS respectively( P 0. 01). Pretreatment with 50 μM propofol reversed H / R-induced neurotoxicity and induced a remarkable increase in NGF mRNA and TrkA mRNA expression and the inhibition of TrkA receptor by K252a( an inhibitor of Trk family members) altered the neuro-protective effect of propofol( P 0. 05 or 0. 01). Conclusion The findings suggest the potential effect of propofol for protecting hippocampal neuron against H / R through NGF / Trk signaling pathway partly.

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Available abstract

Objective To establish a model of hypoxia/re-oxygenation( H/R) injury to examine the neuroprotective effect of propofol,and explore the role of nerve growth factor( NGF) in this action. Methods Hippocampal neurons were randomly assigned to one of 7 groups: Control group( Con group); CoCl2 group; intralipid group( Intra group) : pretreated the neurons with 10% intralipid 90 μL,then added 300 μM CoCl2; propofol group: pretreated the neurons with 10,20,50,100 μM propofol for 1 h,then added 300 μM CoCl2,stimulated with no serum media 24 hours later. MTT method and FACS was used to detect the proliferation and apoptosis of neurons. Then RT-PCR method was used to showthe regulation of NGF and TrkA in propofol preconditioning H / R with different concentrations of propofol. To further investigate the effect of NGF / TrkA signaling pathway,the neurons were stimulated with 1. 0 μmol / LK252 a before treated with 50 μM propofol,expression of TrkA were measured by Western blot. Results H / R resulted in reduced cell viability and increased cell apoptosis in Hippocampal neurons,as indicated by MTT assay and FACS respectively( P 0. 01). Pretreatment with 50 μM propofol reversed H / R-induced neurotoxicity and induced a remarkable increase in NGF mRNA and TrkA mRNA expression and the inhibition of TrkA receptor by K252a( an inhibitor of Trk family members) altered the neuro-protective effect of propofol( P 0. 05 or 0. 01). Conclusion The findings suggest the potential effect of propofol for protecting hippocampal neuron against H / R through NGF / Trk signaling pathway partly.

Key concepts: Propofol, Hippocampal formation, Nerve growth factor, Tropomyosin receptor kinase A, Neuroprotection, Apoptosis, Pharmacology, Chemistry

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