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Verfasst von:Nagel, Simon [VerfasserIn]   i
 Pfleger, Karin [VerfasserIn]   i
 Grond-Ginsbach, Caspar [VerfasserIn]   i
 Wagner, Simone [VerfasserIn]   i
Titel:Suppression of the inflammatory response by diphenyleneiodonium after transient focal cerebral ischemia
Verf.angabe:Simon Nagel, Gina Hadley, Karin Pfleger, Caesar Grond‐Ginsbach, Alastair Mitchell Buchan, Simone Wagner, and Michalis Papadakis
E-Jahr:2012
Jahr:11 October 2012
Umfang:10 S.
Teil:volume:123
 year:2012
 supplement:Suppl. 2
 pages:98-107
 extent:10
Fussnoten:Gesehen am 04.09.2018
Titel Quelle:Enthalten in: Journal of neurochemistry
Ort Quelle:Oxford : Wiley-Blackwell, 1956
Jahr Quelle:2012
Band/Heft Quelle:123(2012), Suppl. 2, Seite 98-107, 10 Seiten
ISSN Quelle:1471-4159
Abstract:Diphenyleneiodonium (DPI), a NADPH oxidase inhibitor, reduces production of reactive oxygen species (ROS) and confers neuroprotection to focal cerebral ischemia. Our objective was to investigate whether the neuroprotective action of DPI extends to averting the immune response. DPI-induced gene changes were analyzed by microarray analysis from rat brains subjected to 90 min of middle cerebral artery occlusion, treated with NaCl (ischemia), dimethylsulfoxide (DMSO), or DMSO and DPI (DPI), and reperfused for 48 h. The genomic expression profile was compared between groups using ingenuity pathway analysis at the pathway and network level. DPI selectively up-regulated 23 genes and down-regulated 75 genes more than twofold compared with both DMSO and ischemia. It significantly suppressed inducible nitric oxide synthase signaling and increased the expression of methionine adenosyltransferasesynthetase 2A and adenosylmethionine decarboxylase 1 genes, which are involved in increasing the production of the antioxidant glutathione. The most significantly affected gene network comprised genes implicated in the inflammatory response with an expression change indicating an overall suppression. Both integrin- and interleukin-17A-signaling pathways were also significantly associated and suppressed. In conclusion, the neuroprotective effects of DPI are mediated not only by suppressing ischemia-triggered oxidative stress but also by limiting leukocyte migration and infiltration.
DOI:doi:10.1111/j.1471-4159.2012.07948.x
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Kostenfrei: Volltext ; Verlag: http://dx.doi.org/10.1111/j.1471-4159.2012.07948.x
 Kostenfrei: Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1471-4159.2012.07948.x
 DOI: https://doi.org/10.1111/j.1471-4159.2012.07948.x
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:diphenyleneiodonium
 focal ischemia
 inflammation
 neuroprotection
 oxidative stress
 stroke
K10plus-PPN:1580647650
Verknüpfungen:→ Zeitschrift

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