Till startsida
Webbkarta
Till innehåll Läs mer om hur kakor används på gu.se

Support for involvement of the renin-angiotensin system in dysplastic Barrett's esophagus

Artikel i vetenskaplig tidskrift
Författare Svein-Olav Bratlie
Anna Casselbrant
Anders Edebo
Lars Fändriks
Publicerad i Scandinavian Journal of Gastroenterology
Volym 52
Nummer/häfte 3
Sidor 338-343
ISSN 0036-5521
Publiceringsår 2017
Publicerad vid Institutionen för kliniska vetenskaper, sektionen för kirurgi och kirurgisk gastroforskning, Avdelningen för gastrokirurgisk forskning och utbildning
Sidor 338-343
Språk English
Länkar dx.doi.org/10.1080/00365521.2016.12...
Ämnesord Barrett's esophagus, biomarker, cancer, endoscopy, renin-angiotensin system, adenocarcinoma incidence, ii receptors, nitric-oxide, cancer, inflammation, expression, diagnosis, pharmacokinetics, guidelines, blockade, Gastroenterology & Hepatology
Ämneskategorier Cancer och onkologi, Klinisk medicin

Sammanfattning

Background and aim: Patients with dysplasia in Barrett's esophagus (BE) have a considerable risk of developing esophageal adenocarcinoma (EAC). The mucosal expression of the pro-inflammatory angiotensin II receptor type 1 (AT1R) is elevated in these patients, suggesting a role in carcinogenesis. The purpose of this study was to determine whether interference with the renin-angiotensin system (RAS) would influence downstream markers of carcinogenesis.Methods: Endoscopic mucosal biopsies from BE patients with low-grade dysplasia (LGD) were sampled before and after a three-week period of RAS-interfering treatment. Thirty patients were randomly allocated to enalapril (ACE inhibitor, 5mg od), candesartan (AT1R antagonist, 8mg od), or no drug. The expression of 12 proteins known to be associated with RAS and carcinogenesis was assessed using western blot.Results: We found altered expression of several proteins after enalapril treatment (decreased: NFB, p=.043; NLRP3, p=.050; AMACR, p=.017; and caspase 3, p=.025; increased: p53, p=.050). Candesartan treatment was associated with increased iNOS expression (p=.033). No significant changes were seen in the no-drug group.Conclusion: Interference with angiotensin II formation was associated with altered expression of inflammation- and carcinogenesis-related proteins. The present results speak in favor of involvement of angiotensin II in BE dysplasia, but the role of AT1R should be investigated further.

Sidansvarig: Webbredaktion|Sidan uppdaterades: 2012-09-11
Dela:

På Göteborgs universitet använder vi kakor (cookies) för att webbplatsen ska fungera på ett bra sätt för dig. Genom att surfa vidare godkänner du att vi använder kakor.  Vad är kakor?