Digitale Bibliotheek
Sluiten Bladeren door artikelen uit een tijdschrift
 
<< vorige    volgende >>
     Tijdschrift beschrijving
       Alle jaargangen van het bijbehorende tijdschrift
         Alle afleveringen van het bijbehorende jaargang
           Alle artikelen van de bijbehorende aflevering
                                       Details van artikel 19 van 32 gevonden artikelen
 
 
  Expression of COX-1, COX-2, iNOS and p38 in Human Brain with Stroke Lesions
 
 
Titel: Expression of COX-1, COX-2, iNOS and p38 in Human Brain with Stroke Lesions
Auteur: Zaher A. Radi
Nasir K. Khan
Verschenen in: International journal of pharmacology
Paginering: Jaargang 4 (2008) nr. 2 pagina's 108-113
Jaar: 2008
Inhoud: The expression profile of COX-1, COX-2, iNOS and p38, in both the normal and post-ischemic human brain was studied. Focal cerebral ischemia is associated with a marked inflammatory reaction that contributes to the evolution and progression of brain tissue injury. Studies employing anti-inflammatory compounds and transgenic mouse models have suggested that both cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) mediate the deleterious effects of ischemic brain injury. A potential role for the mitogen-activated protein kinase (MAPK) p38 in cytokine production following stroke has been hypothesized. In order to evaluate the expression profiles of COX-1, COX-2, iNOS and p38 in normal and post-ischemic human brain, we evaluated the brain tissue from 12 patients with a pathological diagnosis of cerebrovascular disease (CVD) or cerebrovascular accident (CVA) for expression of COX-1, COX-2, p38 and iNOS via immunohistochemistry (IHC) and in situ hybridization (ISH). Corresponding brain sections from six normal patients served as controls. COX-1, COX-2 and iNOS were all present in the normal brain. However, in infarcted brains, an increase in iNOS and COX-2 expression was observed, with no concomitant change in COX-1 staining or p38 noted. Our data demonstrate up-regulation of both iNOS and COX-2, but not p38 or COX-1, in infarcted brains, bolstering the hypothesis that iNOS, COX-2 and their reaction products contribute to the progression of post-ischemic cerebral injury via cytotoxic, rather than cerebrovascular mechanisms.
Uitgever: Asian Network for Scientific Information (provided by DOAJ)
Bronbestand: Elektronische Wetenschappelijke Tijdschriften
 
 

                             Details van artikel 19 van 32 gevonden artikelen
 
<< vorige    volgende >>
 
 Koninklijke Bibliotheek - Nationale Bibliotheek van Nederland