title: [Antagonism effect of MK801 on apoptosis of primary-cultured cortical neuron caused by dimethoate].
abstract: OBJECTIVE
  To explore the antagonism effect of MK801 on apoptosis of primary-cultured cortical neurons caused by dimethoate.
  
  
  METHODS
  Cortical neurons were isolated and cultured in serum free medium for 6 days in vitro, then treated with 100 micromol/L dimethoate for 48h. 50 and 100 micromol/L MK801, a N-methyl-D-aspartic acid receptor (NMDAR) blocker, were used to intervene 100 micromol/L dimethoate group. HPLC-FLD was taken to measure the concentration of excitatory amino acid. RT-PCR was used to detect transcription level of NR2B. Florescence probe DCFH-DA kit was used to detect ROS level. TUNEL staining was used to determine apoptosis.
  
  
  RESULTS
  When neurons were treated with 50 and 100 micromol/L MK801 to 100 micromol/L dimethoate group, Apoptosis decreased to 79.6% of 100 micromol/L dimethoate group in higher intervention group (P < 0.01). Concentration of EAA decreased in both intervention groups (P < 0.01). The level of ROS decreased to 88.9% and 74. 8% of 100 micromol/L dimethoate group (P < 0.01), while still higher than that of control group (P < 0.01). Transcription level of NR2B increased to 1.59 and 2.22 folds of 100 micromol/L dimethoate group (P < 0.01) and had big differences with control group (P < 0.01).
  
  
  CONCLUSIONS
  Excitatory amino acid system and ROS both contribute to the apoptosis of neurons caused by dimethoate. MK801 not only decrease the ROS level but also diminish the elevated excitatory amino acid concentration caused by dimethoate, thus abolish apoptosis of neuron.
authors: School of Public Health/ MOE Key Lab for Public Health/WHO Collaborating Center for Occupational Health, Fudan University, Shanghai 200032, China. hongmei.cui76@gmail.com
authors: Hongmei
authors: H
authors: Cui
authors: Xiuli
authors: X
authors: Chang
authors: Fu
authors: F
authors: Xu
authors: Qing
authors: Q
authors: Wu
authors: Zhijun
authors: Z
authors: Zhou
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000187:drug effects*; D002540:Cerebral Cortex / Q000166:cytology; D004117:Dimethoate / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D016291:Dizocilpine Maleate / Q000494:pharmacology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018846:Excitatory Amino Acids / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000187:drug effects*; D018696:Neuroprotective Agents / Q000494:pharmacology; D061251:Primary Cell Culture; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism
chemical_list: D018691:Excitatory Amino Acid Antagonists; D018846:Excitatory Amino Acids; C121001:NR2B NMDA receptor; D018696:Neuroprotective Agents; D017382:Reactive Oxygen Species; D016194:Receptors, N-Methyl-D-Aspartate; D016291:Dizocilpine Maleate; D004117:Dimethoate