title: Dynamic Regulation of Delta-Opioid Receptor in Rat Trigeminal Ganglion Neurons by Lipopolysaccharide-induced Acute Pulpitis.
abstract: BACKGROUND
  Delta-opioid receptor (DOR) and its endogenous ligands distribute in trigeminal system and play a very important role in modulating peripheral inflammatory pain. DOR activation can trigger p44/42 mitogen-activated protein kinase (ERK1/2) and Akt signaling pathways, which participate in anti-inflammatory and neuroprotective effects. In this study, our purpose was to determine the dynamic changes of DOR in trigeminal ganglion (TG) neurons during the process of acute dental pulp inflammation and elucidate its possible mechanism.
  
  
  METHODS
  Forty rats were used to generate lipopolysaccharide-induced acute pulpitis animal models at 6, 12, and 24 hours and sham-operated groups. Acute pulpitis was confirmed by hematoxylin-eosin staining, and TG neuron activation was determined by anti-c-Fos immunohistochemistry. DOR protein and gene expression in TG was investigated by immunohistochemistry, Western blotting, and real-time polymerase chain reaction, and DOR expression in trigeminal nerves and dental pulp was also determined by immunohistochemistry. To further investigate the mechanism of DOR modulating acute inflammation, the change of pErk1/2 and pAkt in TG was examined by immunohistochemistry.
  
  
  RESULTS
  Lipopolysaccharide could successfully induce acute pulpitis and activated TG neurons. Acute pulpitis could dynamically increase DOR protein and gene expression at 6, 12, and 24 hours in TG, and DOR dimerization was significantly increased at 12 and 24 hours. Acute pulpitis also induced the dynamic change of DOR protein in trigeminal nerve and dental pulp. Furthermore, ERK1/2 and Akt signaling pathways were inhibited in TG after acute pulpitis.
  
  
  CONCLUSIONS
  Increased DOR expression and dimerization may play important roles in peripheral acute inflammatory pain.
authors.affiliation: Department of Neurobiology, Key Laboratory of Neurodegenerative Diseases of Liaoning Province, Liaoning Medical University, Jinzhou, Liaoning, People's Republic of China.
authors.forename: Jin
authors.initials: J
authors.lastname: Huang
authors.affiliation: Department of Neurobiology, Key Laboratory of Neurodegenerative Diseases of Liaoning Province, Liaoning Medical University, Jinzhou, Liaoning, People's Republic of China.
authors.forename: Yiheng
authors.initials: Y
authors.lastname: Lv
authors.affiliation: Department of Neurobiology, Key Laboratory of Neurodegenerative Diseases of Liaoning Province, Liaoning Medical University, Jinzhou, Liaoning, People's Republic of China.
authors.forename: Yunjie
authors.initials: Y
authors.lastname: Fu
authors.affiliation: Department of Neurobiology, Key Laboratory of Neurodegenerative Diseases of Liaoning Province, Liaoning Medical University, Jinzhou, Liaoning, People's Republic of China.
authors.forename: Lili
authors.initials: L
authors.lastname: Ren
authors.affiliation: Department of Neurobiology, Key Laboratory of Neurodegenerative Diseases of Liaoning Province, Liaoning Medical University, Jinzhou, Liaoning, People's Republic of China.
authors.forename: Pan
authors.initials: P
authors.lastname: Wang
authors.affiliation: School of Stomatology, Liaoning Medical University, Jinzhou, Liaoning, People's Republic of China.
authors.forename: Baozhu
authors.initials: B
authors.lastname: Liu
authors.affiliation: School of Stomatology, Liaoning Medical University, Jinzhou, Liaoning, People's Republic of China.
authors.forename: Keqiang
authors.initials: K
authors.lastname: Huang
authors.affiliation: Department of Neurobiology, Key Laboratory of Neurodegenerative Diseases of Liaoning Province, Liaoning Medical University, Jinzhou, Liaoning, People's Republic of China. Electronic address: bijing@lnmu.edu.cn.
authors.forename: Jing
authors.initials: J
authors.lastname: Bi
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D008070:Lipopolysaccharides; D008297:Male; D009474:Neurons / Q000378:metabolism; D011671:Pulpitis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D017207:Rats, Sprague-Dawley; D017465:Receptors, Opioid, delta / Q000378:metabolism*; D015398:Signal Transduction; D012668:Trigeminal Ganglion / Q000378:metabolism*
chemical_list: D008070:Lipopolysaccharides; D017465:Receptors, Opioid, delta
keywords: Acute pulpitis; pAkt (Ser473); pERK1/2; rat; trigeminal ganglion; δ-opioid receptor