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Open Access Research article

Anti-inflammatory effects of Neurotoxin-Nna, a peptide separated from the venom of Naja naja atra

Yeping Ruan1*, Li Yao1, Bingbing Zhang1, Shuijuan Zhang1 and Jianyou Guo2*

Author Affiliations

1 College of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, P.R China

2 Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences, Beijing, 100101, P.R China

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BMC Complementary and Alternative Medicine 2013, 13:86  doi:10.1186/1472-6882-13-86

Published: 15 April 2013

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.

Keywords:
Neurotoxin-Nna; Anti-inflammatory; Antinociceptive; Tumor necrosis factor alpha; Interleukin 1 beta; Nuclear factor kappa B