title: [Apoptosis of neuroglial cell and expressions of neurite outgrowth inhibitor B and MAP kinase-activated protein kinase 2 in white matter damage model of newborn rat brain].
abstract: OBJECTIVE
  To observe and explore the apoptosis of neuroglial cell and the expression changes of neurite outgrowth inhibitor B (Nogo-B) and MAP kinase-activated protein kinase 2 (MK2) in SD rats with white matter damage (WMD).
  
  
  METHODS
  The WMD model of newborn rat was established for this study, and then the pups were respectively killed at 30 min, 1 h, 4 h, 12 h, 1 d, 3 d, 7 d, 14 d, 21 d after WMD. The apoptosis of neuroglial cells was investigated by TUNEL method; the changes of Nogo-B expression in white matter were investigated by immunohistochemical technique; the changes of expression of MK2 mRNA in white matter were measured by in situ hybridization.
  
  
  RESULTS
  TUNEL result showed the number of apoptotic cells increased at 4 h and peaked at 3 d, decreased at 7 d after WMD of newborn rat; the expression of MK2 mRNA began to increase at 1 h and reached a maximum at 3 d (P<0.05); the expression of Nogo-B in periventricular white matter and corpus callosum of WMD rat was up-regulated at 12 h and peaked at 3 d after cerebral white matter damage, displaying significant differences at 12 h, 1 d, 3 d and 7 d when the Nogo-B expression in WMD rat compared with that observed in the control (P<0.05).
  
  
  CONCLUSIONS
  Nogo-B and MK2 can participate in pathogenesis of white matter damage in newborn rat.
authors.affiliation: Department of Pediatrics, West China Second Hospital, Sichuan University, Chengdu 610041, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Yang
authors.forename: Ying
authors.initials: Y
authors.lastname: Xiong
authors.forename: Lin
authors.initials: L
authors.lastname: Qin
authors.forename: Ping-Hui
authors.initials: PH
authors.lastname: Zhuo
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D005260:Female; D020925:Hypoxia-Ischemia, Brain / Q000503:physiopathology*; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D020287:In Situ Nick-End Labeling; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics*; D008297:Male; D009185:Myelin Proteins / Q000096:biosynthesis*; D009457:Neuroglia / Q000378:metabolism* / Q000473:pathology; D000070798:Nogo Proteins; D017346:Protein Serine-Threonine Kinases / Q000235:genetics*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D000099190:MAP-Kinase-Activated Kinase 2
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D009185:Myelin Proteins; D000070798:Nogo Proteins; D017346:Protein Serine-Threonine Kinases; D012333:RNA, Messenger; D000099190:MAP-Kinase-Activated Kinase 2; C000603197:Rtn4 protein, rat