Acrylamide has been shown to be neurotoxic.Brain-derived neurotrophic factor(BDNF)can alleviate acrylamide-induced synaptic injury;however,the underlying mechanism remains unclear.In this study,dibutyryl-cyclic adenos...Acrylamide has been shown to be neurotoxic.Brain-derived neurotrophic factor(BDNF)can alleviate acrylamide-induced synaptic injury;however,the underlying mechanism remains unclear.In this study,dibutyryl-cyclic adenosine monophosphate-induced mature human neuroblastoma(NB-1)cells were exposed with 0–100μg/mL acrylamide for 24–72 hours.Acrylamide decreased cell viability and destroyed synapses.Exposure of co-cultured NB-1 cells and Schwann cells to 0–100μg/mL acrylamide for 48 hours resulted in upregulated expression of synapsin I and BDNF,suggesting that Schwann cells can activate self-protection of neurons.Under co-culture conditions,activation of the downstream TrkB-MAPK-Erk1/2 pathway strengthened the protective effect.Exogenous BDNF can increase expression of TrkB,Erk1/2,and synapsin I,while exogenous BDNF or the TrkB inhibitor K252a could inhibit these changes.Taken together,Schwann cells may act through the BDNF-TrkB-MAPK-Erk1/2 signaling pathway,indicating that BDNF plays an important role in this process.Therefore,exogenous BDNF may be an effective treatment strategy for acrylamide-induced nerve injury.This study was approved by the Laboratory Animal Welfare and Ethics Committee of the National Institute of Occupational Health and Poison Control,a division of the Chinese Center for Disease Control and Prevention(approval No.EAWE-2017-008)on May 29,2017.展开更多
基金This study was supported by the National Natural Science Foundation of China,Nos.81773474 and 81273110(to BL)the National Key Research and Development Project of China,No.2017YFF0211201(to BL).
文摘Acrylamide has been shown to be neurotoxic.Brain-derived neurotrophic factor(BDNF)can alleviate acrylamide-induced synaptic injury;however,the underlying mechanism remains unclear.In this study,dibutyryl-cyclic adenosine monophosphate-induced mature human neuroblastoma(NB-1)cells were exposed with 0–100μg/mL acrylamide for 24–72 hours.Acrylamide decreased cell viability and destroyed synapses.Exposure of co-cultured NB-1 cells and Schwann cells to 0–100μg/mL acrylamide for 48 hours resulted in upregulated expression of synapsin I and BDNF,suggesting that Schwann cells can activate self-protection of neurons.Under co-culture conditions,activation of the downstream TrkB-MAPK-Erk1/2 pathway strengthened the protective effect.Exogenous BDNF can increase expression of TrkB,Erk1/2,and synapsin I,while exogenous BDNF or the TrkB inhibitor K252a could inhibit these changes.Taken together,Schwann cells may act through the BDNF-TrkB-MAPK-Erk1/2 signaling pathway,indicating that BDNF plays an important role in this process.Therefore,exogenous BDNF may be an effective treatment strategy for acrylamide-induced nerve injury.This study was approved by the Laboratory Animal Welfare and Ethics Committee of the National Institute of Occupational Health and Poison Control,a division of the Chinese Center for Disease Control and Prevention(approval No.EAWE-2017-008)on May 29,2017.
