Tissue xanthine oxidase activity and nitric oxide levels after spinal cord ischemia/reperfusion injury in rabbits
dc.authorwosid | Uz, Efkan/B-2943-2016 | |
dc.contributor.author | Sahin, S | |
dc.contributor.author | Sögüt, S | |
dc.contributor.author | Özyurt, H | |
dc.contributor.author | Uz, E | |
dc.contributor.author | Ilhan, A | |
dc.contributor.author | Akyol, Ö | |
dc.date.accessioned | 2024-08-04T20:13:09Z | |
dc.date.available | 2024-08-04T20:13:09Z | |
dc.date.issued | 2002 | |
dc.department | İnönü Üniversitesi | en_US |
dc.description.abstract | Caffeic acid phenethyl ester exhibits antioxidant properties. This experimental study was designed to determine the effect of CAPE on nitric NO level and XO activity after reperfusion injury of spinal cord. New Zealand white rabbits were undergone aortic occlusion. CAPE, methylprednisolone or saline were injected intraperitoneally before surgical intervention. Animals were subjected to 21 min of crossclamp time. At the end of occlusion time, the clamps were removed and restoration of the blood flow was verified visually. Animals in sham group underwent a surgical procedure similar to the other groups but the aorta was not occluded. Spinal cord specimens were obtained to determine the tissue levels of NO and XO activity. Both XO activity and NO level in ischemia group were significantly higher than those of sham group (p = 0.0005 and 0.0003, respectively). MP and CAPE had no effect on XO activity after reperfusion. These two agents decreased NO levels nearly to that of sham group after reperfusion. There were no differences between MP and CAPE on reducing NO level. These results suggest that rabbits with ischemia-reperfusion injury in spinal cord have increased cord concentrations of nitrite and nitrate that are indicative of endogenous overproduction of NO. CAPE may be regarded as an agent that protects spinal cord from ischemia-reperfusion injury. | en_US |
dc.identifier.doi | 10.1002/nrc.10044 | |
dc.identifier.endpage | 121 | en_US |
dc.identifier.issn | 0893-6609 | |
dc.identifier.issue | 2 | en_US |
dc.identifier.scopus | 2-s2.0-0036754649 | en_US |
dc.identifier.scopusquality | N/A | en_US |
dc.identifier.startpage | 111 | en_US |
dc.identifier.uri | https://doi.org/10.1002/nrc.10044 | |
dc.identifier.uri | https://hdl.handle.net/11616/93438 | |
dc.identifier.volume | 31 | en_US |
dc.identifier.wos | WOS:000178925700006 | en_US |
dc.identifier.wosquality | Q4 | en_US |
dc.indekslendigikaynak | Web of Science | en_US |
dc.indekslendigikaynak | Scopus | en_US |
dc.language.iso | en | en_US |
dc.publisher | Wiley | en_US |
dc.relation.ispartof | Neuroscience Research Communications | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | caffeic acid phenethyl ester | en_US |
dc.subject | methylprednisolone | en_US |
dc.subject | spinal cord | en_US |
dc.subject | reperfusion injury | en_US |
dc.subject | xanthine oxidase | en_US |
dc.subject | nitric oxide | en_US |
dc.title | Tissue xanthine oxidase activity and nitric oxide levels after spinal cord ischemia/reperfusion injury in rabbits | en_US |
dc.type | Article | en_US |