Abstract | BACKGROUND: Persistent pain resulting from peripheral injury/ inflammation is associated with altered sensitivity to cutaneous stimuli, which can manifest as hyperalgesia. The role of oxidant stress in the development, progression and maintenance of hyperalgesia is still not understood. Furthermore, there appears to be a relationship between c-Src kinase in the pain pathway and oxidative stress. METHODS: RESULTS: PP2 and c-Src siRNA attenuated PPC-induced thermal hyperalgesia, while SSG enhanced it. AG 1478 had no effect. PP2 decreased the levels of IL-1β, c-Src/inhibitory kappa B kinase complex formed and prostaglandin E2 produced in the dorsal root ganglia (DRG) ipsilateral to the inflamed paw, while SSG increased the levels of these parameters. c-Src siRNA decreased Src expression and activity in the DRG ipsilateral to the inflamed paw. CONCLUSIONS: These results confirm that prooxidant-activated c-Src plays a role in initiating and maintaining hyperalgesia by regulating a stimulus-response coupling between the inflamed tissue and the DRG in the pain pathway. Our data also suggest that oxidant-induced dysregulation of c-Src/ nuclear factor kappa B coupling may contribute to our understanding of the transition from acute to chronic dysfunctional pain state seen in many human diseases.
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Authors | O J Igwe |
Journal | European journal of pain (London, England)
(Eur J Pain)
Vol. 17
Issue 7
Pg. 1027-38
(Aug 2013)
ISSN: 1532-2149 [Electronic] England |
PMID | 23280824
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Copyright | © 2012 European Federation of International Association for the Study of Pain Chapters. |
Chemical References |
- Chromates
- Enzyme Inhibitors
- NF-kappa B
- Peroxides
- potassium tetraperoxochromate
- src-Family Kinases
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Topics |
- Animals
- Chromates
(pharmacology)
- Disease Models, Animal
- Enzyme Inhibitors
(pharmacology)
- Ganglia, Sensory
(metabolism)
- Ganglia, Spinal
(drug effects, metabolism)
- Hyperalgesia
(metabolism, physiopathology)
- Inflammation
(chemically induced, metabolism, physiopathology)
- Male
- NF-kappa B
(metabolism)
- Pain
(chemically induced, metabolism)
- Peroxides
(pharmacology)
- Rats
- Rats, Sprague-Dawley
- Signal Transduction
(drug effects)
- src-Family Kinases
(metabolism)
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