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Involvement of the nitric oxide–cyclic GMP–protein kinase G–K+ channel pathway in the antihyperalgesic effects of bovine lactoferrin in a model of neuropathic pain
- Source :
-
Brain Research . May2008, Vol. 1209, p1-7. 7p. - Publication Year :
- 2008
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Abstract
- Abstract: The possible involvement of the nitric oxide (NO)–cyclic GMP (cGMP)–protein kinase G (PKG) pathway on bovine lactoferrin (BLF)-induced spinal antihyperalgesic activity was elucidated in sciatic nerve injured rats. Intrathecal BLF reduced thermal hyperalgesia in a dose-dependent manner. Pretreatment with N G-l-nitro-arginine methyl ester (l-NAME, non-specific inhibitor of NO synthase), 7-nitroindazole (7-NI, neuronal NO synthase inhibitor), 1H-[1,2,4]-oxadiazolo [4,3-a] quinoxalin-1-one (ODQ, guanylyl-cyclase inhibitor), (9S, 10R, 12R)-2,3,9,10,11,12-hexahydro-10-methoxy-2, 9-dimethyl-1-oxo-9, 12-epoxy-1H-diindolo-[1,2,3-fg:3′,2′,1′-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester (KT-5823, specific PKG inhibitor) or glybenclamide (ATP-sensitive K+ channel blocker), but not N G-d-nitro-arginine methyl ester (d-NAME, an inactive enantiomer of l-NAME), d-Phe-Cys-Tyr-d-Trp-Orn-Thr-NH2 (CTOP, selective μ-opioid receptor antagonist) or naloxone (nonselective opioid receptor antagonist) prevented BLF-induced antihyperalgesia. Data suggest that BLF-induced spinal antihyperalgesia could be due to activation of the NO–cGMP–PKG–K+ channel pathway and it is not mediated by μ-opioid receptor in a model of neuropathic pain. [Copyright &y& Elsevier]
- Subjects :
- *NITRIC oxide
*NITROGEN compounds
*OXIDES
*PROTEIN kinases
Subjects
Details
- Language :
- English
- ISSN :
- 00068993
- Volume :
- 1209
- Database :
- Academic Search Index
- Journal :
- Brain Research
- Publication Type :
- Academic Journal
- Accession number :
- 32030383
- Full Text :
- https://doi.org/10.1016/j.brainres.2008.03.004