Abstract | BACKGROUND:
Najanalgesin, a toxin isolated from the venom of Naja naja atra, has been shown to exert significant analgesic effects in a neuropathic pain model in rats. However, the molecular mechanism underlying this protective effect of najanalgesin is poorly understood. The present study sought to evaluate the intracellular signaling pathways that are involved in the antinociceptive effect of najanalgesin on neuropathic pain. METHODS: RESULTS: The phosphorylation levels of JNK (as well as its downstream molecule c-Jun), p38, and ERK were significantly increased after injury. Najanalgesin only inhibited JNK and c-Jun phosphorylation but had no effect on either ERK or p38. This inhibition of JNK was confirmed by immunohistochemistry, which suggested that the antinociceptive effect of najanalgesin on spinal nerve ligation-induced neuropathic pain in rats is associated with JNK activation in the spinal cord. CONCLUSION:
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Authors | Ying-Xia Liang, Zhi-Yu Zhang, Rui Zhang |
Journal | Chinese medical journal
(Chin Med J (Engl))
Vol. 128
Issue 17
Pg. 2340-5
(Sep 05 2015)
ISSN: 2542-5641 [Electronic] China |
PMID | 26315082
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Elapid Venoms
- Proto-Oncogene Proteins c-jun
- najanalgesin
- Extracellular Signal-Regulated MAP Kinases
- JNK Mitogen-Activated Protein Kinases
- p38 Mitogen-Activated Protein Kinases
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Topics |
- Animals
- Elapid Venoms
(therapeutic use)
- Extracellular Signal-Regulated MAP Kinases
(genetics, metabolism)
- Immunohistochemistry
- JNK Mitogen-Activated Protein Kinases
(genetics, metabolism)
- Male
- Neuralgia
(drug therapy, enzymology)
- Proto-Oncogene Proteins c-jun
(genetics, metabolism)
- Rats
- Rats, Sprague-Dawley
- p38 Mitogen-Activated Protein Kinases
(genetics, metabolism)
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