title: [Effects of 12/15-lipoxygenase antisense oligonucleotide on peroxisome proliferator-activated receptor γ translocation in primarily cultured cortical neurons after oxygen-glucose deprivation].
abstract: OBJECTIVE
  To explore the effects of 12/15-lipoxygenase antisense oligonucleotide (asON-12/15-LOX) on OGD (oxygen-glucose deprivation)-induced PPARγ (peroxisome proliferator-activated receptor γ) expression and nuclear translocation in primarily cultured cortical neurons.
  
  
  METHODS
  After a 48-h pre-treatment of 12/15-LOX antisense oligonucleotide (asON), primarily cultured cortical neurons underwent 3-hour OGD followed by a 24-hour reperfusion.Immunofluorescent staining and Western blot were used to evaluate the expressions of 12/15-LOX and PPARγ as well as the nuclear translocation of PPARγ.
  
  
  RESULTS
  Compared with the control group, the expressions of 12/15-LOX and PPARγ whole protein were enhanced in OGD group (t = -3.72 and -6.79, P = 0.03 and 0.04). And an increase of PPARγ in nucleus (t = -4.67, P = 0.02) could be noted with a simultaneous reduction in cytosol (t = 3.40, P = 0.04) after OGD, indicating an induction of nuclear translocation by OGD. Compared with OGD group, a pre-treatment of asON-12/15-LOX dramatically attenuated OGD-induced increase in 12/15-LOX whole protein expression (t = 5.03, P = 0.02). Compared with OGD group, a pre-treatment of asON-12/15-LOX greatly reduced OGD-induced increase in PPARγ total protein expression (t = 2.83, P = 0.04) and nuclear translocation (t = 7.05, P = 0.01 for nuclear protein; t = -5.47, P = 0.01 for cytosol protein). It indicated a possible link between 12/15-LOX and PPARγ.
  
  
  CONCLUSIONS
  12/15-LOX antisense oligonucleotide suppresses the expression and nuclear translocation of PPARγ in primarily cultured cortical neurons after OGD.
authors.affiliation: Department of Neurology, Tianjin Medical University General Hospital, Tianjin 300052, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Han
authors.affiliation: Department of Neurology, Tianjin Medical University General Hospital, Tianjin 300052, China. Email: sunli_2000@hotmail.com.
authors.forename: Li
authors.initials: L
authors.lastname: Sun
authors.affiliation: Department of Neurology, Tianjin Medical University General Hospital, Tianjin 300052, China.
authors.forename: Hao
authors.initials: H
authors.lastname: Liang
authors.affiliation: Department of Neurology, Tianjin Medical University General Hospital, Tianjin 300052, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Cheng
mesh_terms: D000818:Animals; D001092:Arachidonate 12-Lipoxygenase / Q000494:pharmacology*; D001093:Arachidonate 15-Lipoxygenase / Q000494:pharmacology*; D015687:Cell Hypoxia; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology; D003470:Culture Media / Q000737:chemistry; D005947:Glucose / Q000737:chemistry; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D016376:Oligonucleotides, Antisense / Q000494:pharmacology*; D010100:Oxygen / Q000737:chemistry; D047495:PPAR gamma / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: C475064:12-15-lipoxygenase; D003470:Culture Media; D016376:Oligonucleotides, Antisense; D047495:PPAR gamma; D001092:Arachidonate 12-Lipoxygenase; D001093:Arachidonate 15-Lipoxygenase; D005947:Glucose; D010100:Oxygen