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Bee venom injection produces a peripheral anti-inflammatory effect by activation of a nitric oxide-dependent spinocoeruleus pathway

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dc.contributor.authorYoon, Seo Yeon-
dc.contributor.authorKwon, Young-Bae-
dc.contributor.authorKim, Hyun-Woo-
dc.contributor.authorRoh, Dae-Hyun-
dc.contributor.authorSeo, Hyoung-Sig-
dc.contributor.authorHan, Ho-Jae-
dc.contributor.authorLee, Hye-Jung-
dc.contributor.authorBeitze, Alvin J.-
dc.contributor.authorLee, Jang-Hern-
dc.date.accessioned2009-08-21T08:36:26Z-
dc.date.available2009-08-21T08:36:26Z-
dc.date.issued2007-11-05-
dc.identifier.citationNeurosci. Lett. 430 (2008) 163-168en
dc.identifier.issn0304-3940-
dc.identifier.urihttp://hdl.handle.net/10371/7481-
dc.description.abstractOur recent data, obtained using a zymosan-induced inflammatory air pouch model in mice, have demonstrated that subcutaneous bee venom (BV) injection into the hind limb selectively activates the contralateral brain stem locus coeruleus (LC) and then via a descending noradrenergic pathway and subsequent adrenal medullary catecholamine release induces a potent anti-inflammatory effect. While the efferent limb of this BV-induced neuroimmune anti-inflammatory pathway is well documented, the afferent limb of this pathway is poorly understood. In particular the spinal mechanisms involved with BV activation of the LC are currently unknown. Spinal nitric oxide (NO) and its synthase (NOS) have been shown to play an important role in the transmission and amplification of neuronal information from the spinal cord to the brain stem. In the present study we evaluated whether spinal NO plays a role in BV-induced LC activation, since we have previously shown that LC activation underlies this ‘BV-induced anti-inflammatory effect’ (BVAI) using the mouse air pouch model. Intrathecal (i.t.) pretreatment with l-nitro arginine methyl ester (l-NAME, non-selective NOS inhibitor), hemoglobin (NO scavenger) or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, soluble guanylate cyclase inhibitor) abolished BVAI on zymosan-induced leukocyte migration into the air pouch. Moreover, i.t. injection of l-N-iminoethyl-lysine (l-NIL, inducible NOS inhibitor), but not 7-nitroindazole (7-NI, neuronal NOS inhibitor), also inhibited BVAI. BV injection significantly increased both the number of Fos immunoreactive neurons and tyrosine hydroxylase-Fos double labeling neurons in the contralateral LC in zymosan-induced inflamed mice. Importantly this increase in Fos expression in the LC was also completely inhibited by i.t. injection of l-NIL, but not by i.t. injection of 7-NI. Collectively these results indicate that spinal NO generated from inducible NOS is involved in the BV-induced LC activation that underlies BVAI.en
dc.description.sponsorshipThis study was supported by a grant (M103KV010009-03K2201-00940) from the Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology of the Republic of Korea. This work was also supported by the SRC/ERC program of MOST/KOSEF (R11-2005-014) as well as the Brain Korea 21 project, in the College of Veterinary Medicine, Chonnam National University, Korea.en
dc.language.isoen-
dc.publisherElsevieren
dc.subjectBee venomen
dc.subjectInflammationen
dc.subjectNitric oxide synthaseen
dc.subjectLocus coeruleusen
dc.subjectSpinal corden
dc.subjectNeuroimmune modulationen
dc.titleBee venom injection produces a peripheral anti-inflammatory effect by activation of a nitric oxide-dependent spinocoeruleus pathwayen
dc.typeArticleen
dc.contributor.AlternativeAuthor윤서연-
dc.contributor.AlternativeAuthor권영배-
dc.contributor.AlternativeAuthor김현우-
dc.contributor.AlternativeAuthor노대현-
dc.contributor.AlternativeAuthor서형식-
dc.contributor.AlternativeAuthor한호재-
dc.contributor.AlternativeAuthor이혜정-
dc.contributor.AlternativeAuthor이장헌-
dc.identifier.doi10.1016/j.neulet.2007.10.035-
Appears in Collections:
College of Veterinary Medicine (수의과대학)Dept. of Veterinary Medicine (수의학과)Journal Papers (저널논문_수의학과)
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