title: Anti-inflammatory effects of Neurotoxin-Nna, a peptide separated from the venom of Naja naja atra.
abstract: BACKGROUND
  Neurotoxin-Nna (NT), an analgesic peptide separated from the venom of Naja naja atra, has reported to have an exceptional specificity to block transmission of the nerve impulse by binding to the α- subunit of the nicotinic acetylcholine receptor in the membrane. However, little information is available on the anti-inflammatory effects of NT. Therefore, the anti-inflammatory activity of Neurotoxin-Nna was investigated in this study.
  
  
  METHODS
  The anti-inflammatory effects of NT were evaluated by measuring its influence on several crucial factors in inflammatory pathways, including total antioxidant activity, antinociceptive effects in vivo, nuclear factor kappa B (NF-κB), polymorphonuclear cells (PMN), inducible nitric oxide synthase (iNOS), adhesion molecule (ICAM-1) and tactile hyperalgesia.
  
  
  RESULTS
  NT treatment decreased the levels of tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β). NT treatment decreased the total antioxidant status (TAOS) and reduced CFA-induced tactile hyperalgesia in a dose-dependent manner. NT significantly inhibited regulation of NF-kappaB activation and the production of IL-1β, TNF-α, iNOS and CAM-1. Moreover, NT suppressed infiltration of PMN.
  
  
  CONCLUSIONS
  Our results showed that NT reduced CFA-induced tactile hyperalgesia through inhibition inflammatory pathways in experimental inflammatory rats.
authors.affiliation: College of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, PR China. yepingruan@yeah.net
authors.forename: Yeping
authors.initials: Y
authors.lastname: Ruan
authors.forename: Li
authors.initials: L
authors.lastname: Yao
authors.forename: Bingbing
authors.initials: B
authors.lastname: Zhang
authors.forename: Shuijuan
authors.initials: S
authors.lastname: Zhang
authors.forename: Jianyou
authors.initials: J
authors.lastname: Guo
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage* / Q000737:chemistry / Q000302:isolation & purification; D003039:Cobra Neurotoxin Proteins / Q000008:administration & dosage* / Q000737:chemistry / Q000302:isolation & purification; D004546:Elapid Venoms / Q000737:chemistry*; D017815:Elapidae; D005260:Female; D006801:Humans; D006930:Hyperalgesia / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000276:immunology; D053583:Interleukin-1beta / Q000235:genetics / Q000276:immunology; D008297:Male; D016328:NF-kappa B / Q000235:genetics / Q000276:immunology; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000276:immunology; D010455:Peptides / Q000008:administration & dosage* / Q000737:chemistry / Q000302:isolation & purification; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
chemical_list: D000893:Anti-Inflammatory Agents; D003039:Cobra Neurotoxin Proteins; D004546:Elapid Venoms; D053583:Interleukin-1beta; D016328:NF-kappa B; D010455:Peptides; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D052247:Nitric Oxide Synthase Type II