Neural Regeneration Research ›› 2021, Vol. 16 ›› Issue (1): 150-157.doi: 10.4103/1673-5374.286976

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Brain-derived neurotrophic factor protects against acrylamide-induced neuronal and synaptic injury via the TrkB-MAPK-Erk1/2 pathway

Xiao Chen1, #, Jing-Wei Xiao1, #, Peng Cao1, Yi Zhang1, Wen-Jian Cai1, Jia-Yang Song1, Wei-Min Gao2, *, Bin Li1, *   

  1. 1 Department of Toxicology, Key Lab of Chemical Safety and Health, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China;   2 Department of Occupational and Environmental Health Sciences, School of Public Health, West Virginia University, Morgantown, WV, USA
  • Online:2021-01-15 Published:2020-11-26
  • Contact: Bin Li, MS, binli65111@hotmail.com; Wei-Min Gao, PhD, weimin.gao@hsc.wvu.edu. #Both authors contributed equally to this work.
  • Supported by:
    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).

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Abstract: 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 0–100 μg/mL acrylamide for 24–72 hours. Acrylamide decreased cell viability and destroyed synapses. Exposure of co-cultured NB-1 cells and Schwann cells to 0–100 μg/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.

Key words: factor, injury, pathway, peripheral nerve, protection, protein, regeneration, repair