Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/28266
Title: The role of nitric oxide and other gaseous mediators in cardiovascular disease models; emphasis on septic shock
Authors: FARHANA BINTE MOHAMMED ANUAR
Keywords: nitric oxide, hydrogen sulphide, sepsis, endotoxic shock, NF-kB, proteasome
Issue Date: 10-Dec-2007
Source: FARHANA BINTE MOHAMMED ANUAR (2007-12-10). The role of nitric oxide and other gaseous mediators in cardiovascular disease models; emphasis on septic shock. ScholarBank@NUS Repository.
Abstract: The effect of flurbiprofen (FLU), nitroflurbiprofen (NOF), L-NAME, and 1400W were evaluated in sepsis. In CLP rats, FLU (21mgkg-1,p.o.) or NOF (3-30mgkg-1,p.o.) increased blood pressure, reduced organ damage and prolonged survival time. NOF (but not FLU) significantly reduced plasma TNFa. Neither drug affected plasma IL-1B. In LPS rats (10mgkg-1,i.p.), NOF (3-30mgkg-1,i.p.) gave a dose-dependent inhibition of plasma NOx, TNFa, IL-1B, liver H2S, CBS/CSE mRNA, iNOS, MPO activity, NF-kB and proteasome activation. FLU (21mgkg-1,i.p.) was without effect. L-NAME (25-100mgkg-1,i.p.) gave a dose-dependent increase in the abovementioned indicators except for a dose-dependent inhibition of plasma NOx, eNOS and iNOS. 1400W (1-10mgkg-1,i.p.) gave a dose-dependent inhibition of the abovementioned indicators except for a dose-dependent increase of liver eNOS. Thus both NOF and 1400W are able to downregulate pro-inflammatory H2S most probably via the inhibition of transduction of the proteasome-NF-kB pathway, in turn suggesting the existence of cross talk between NO and H2S.
URI: http://scholarbank.nus.edu.sg/handle/10635/28266
Appears in Collections:Ph.D Theses (Open)

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
Farhana Anuar - The role of NO & other gaseous mediators in septic shock (2007).pdf3.62 MBAdobe PDF

OPEN

NoneView/Download

Page view(s)

200
checked on Dec 11, 2017

Download(s)

251
checked on Dec 11, 2017

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.