scholarly journals Effects of rotenone on inducible nitric oxide synthase and cyclooxygenase-2 mRNA levels detected by real-time PCR in a rat bladder ischemia/reperfusion model

2012 ◽  
Vol 4 (2) ◽  
pp. 344-348 ◽  
Author(s):  
İDRIS NERGIZ ◽  
BARBAROS BAŞESKIOĞLU ◽  
AYDIN YENILMEZ ◽  
NILÜFER ERKASAP ◽  
CAVIT CAN ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Real Time ◽  
Inducible Nitric Oxide Synthase ◽  
Real Time Pcr ◽  
Ischemia Reperfusion ◽  
Mrna Levels ◽  
Oxide Synthase ◽  
Bladder Ischemia ◽  
Inducible Nitric Oxide

Role of TLR-4/IL-6/TNF-α, COX-II and eNOS/iNOS pathways in the impact of carvedilol against hepatic ischemia reperfusion injury

2021 ◽  
pp. 096032712199944
Author(s):  
Mohamed IA Hassan ◽  
Fares EM Ali ◽  
Abdel-Gawad S Shalkami
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Liver Enzymes ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Aim: Hepatic ischemia/reperfusion (I/R) injury is a syndrome involved in allograft dysfunction. This work aimed to elucidate carvedilol (CAR) role in hepatic I/R injury. Methods: Male rats were allocated to Sham group, CAR group, I/R group and CAR plus I/R group. Rats subjected to hepatic ischemia for 30 minutes then reperfused for 60 minutes. Oxidative stress markers, inflammatory cytokines and nitric oxide synthases were measured in hepatic tissues. Results: Hepatocyte injury following I/R was confirmed by a marked increase in liver enzymes. Also, hepatic I/R increased the contents of malondialdehyde however decreased glutathione contents and activities of antioxidant enzymes. Furthermore, hepatic I/R caused elevation of toll-like receptor-4 (TLR-4) expression and inflammatory mediators levels such as tumor necrosis factor-α, interleukin-6 and cyclooxygenase-II. Hepatic I/R caused down-regulation of endothelial nitric oxide synthase and upregulation of inducible nitric oxide synthase expressions. CAR treatment before hepatic I/R resulted in the restoration of liver enzymes. Administration of CAR caused a significant correction of oxidative stress and inflammation markers as well as modulates the expression of endothelial and inducible nitric oxide synthase. Conclusions: CAR protects liver from I/R injury through reduction of the oxidative stress and inflammation, and modulates endothelial and inducible nitric oxide synthase expressions.

scholarly journals Dynamics of Nitrotyrosine Formation and Decay in Rat Brain during Focal Ischemia-Reperfusion

1999 ◽  
Vol 19 (6) ◽  
pp. 667-672 ◽  
Author(s):  
Shunya Takizawa ◽  
Naoto Fukuyama ◽  
Hisayuki Hirabayashi ◽  
Hiroe Nakazawa ◽  
Yukito Shinohara
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Rat Brain ◽  
Inducible Nitric Oxide Synthase ◽  
Time Window ◽  
Ischemia Reperfusion ◽  
Late Phase ◽  
Focal Ischemia ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The purpose of this study was to establish the dynamics of nitrotyrosine (NO2-Tyr) formation and decay during the rise of NO2-Tyr in rat brain subjected to 2-hour focal ischemia-reperfusion, and to evaluate the role of inducible nitric oxide synthase in the rise. The authors first determined the half life of NO2-Tyr in rat brain at 24 hours after the start of reperfusion by blocking NO2-Tyr formation with NG-monomethyl-l-arginine and after the decay of NO2-Tyr by means of a hydrolysis/HPLC procedure. The values obtained were approximately 2 hours in both peri-infarct and core-of-infarct regions. Using the same hydrolysis/HPLC procedure, the ratio of nitrotyrosine to tyrosine from the 2-hour occlusion to as much as 72 hours after the start of reperfusion was measured in the presence and absence of aminoguanidine (100 mg/kg intraperitoneally twice a day). In the absence of aminoguanidine, the ratio of NO2-Tyr in the peri-infarct and core-of-infarct regions reached 0.95% ± 0.34% and 0.52% ± 0.34%, respectively, at 1 hour after the start of reperfusion, The elevated levels persisted until 48 hours, then declined, The peri-infarct region showed the highest percent NO2-Tyr level, followed by the core of infarct, then the caudoputamen, Aminoguanidine significantly reduced NO2-Tyr formation (up to 90% inhibition) during 24 to 48 hours, The authors conclude that inducible nitric oxide synthase is predominantly responsible for NO2-Tyr formation, at least in the late phase of reperfusion, These results have important implications for the therapeutic time window and choice of nitric oxide synthase inhibitors in patients with cerebral infarction.

scholarly journals Inhibition of inducible nitric oxide synthase reduces renal ischemia/reperfusion injury

2002 ◽  
Vol 61 (3) ◽  
pp. 862-871 ◽  
Author(s):  
Prabal K. Chatterjee ◽  
Nimesh S.A. Patel ◽  
Espen O. Kvale ◽  
Salvatore Cuzzocrea ◽  
Paul A.J. Brown ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Reperfusion Injury ◽  
Inducible Nitric Oxide Synthase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

LPS-induced downregulation of MRP2 and BSEP in human liver is due to a posttranscriptional process

2004 ◽  
Vol 287 (5) ◽  
pp. G1008-G1016 ◽  
Author(s):  
Marieke G. L. Elferink ◽  
Peter Olinga ◽  
Annelies L. Draaisma ◽  
Marjolijn T. Merema ◽  
Klaas Nico Faber ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Rat Liver ◽  
Inducible Nitric Oxide Synthase ◽  
Human Liver ◽  
Mrna Levels ◽  
Liver Slices ◽  
Oxide Synthase ◽  
Human Liver Slices ◽  
Inducible Nitric Oxide

Endotoxin-induced cholestasis in rodents is caused by hepatic downregulation of transporters, including the basolateral Na+-dependent taurocholate transporter (ntcp) and the canalicular bile salt export pump (bsep) and multidrug resistance-associated protein 2 (mrp2). Details about the regulation of the human transporter proteins during this process are lacking. We used precision-cut human and rat liver slices to study the regulation of transporter expression during LPS-induced cholestasis. We investigated the effect of LPS on nitrate/nitrite and cytokine production in relation to the expression of inducible nitric oxide synthase, NTCP, BSEP, and MRP2 both at the level of mRNA with RT-PCR and protein using immunofluorescence microscopy. In liver slices from both species, LPS-induced expression of inducible nitric oxide synthase was detected within 1–3 h and remained increased over 24 h. In rat liver slices, this was accompanied by a significant decrease of rat ntcp and mrp2 mRNA levels, whereas bsep levels were not affected. These results are in line with previous in vivo studies and validate our liver slice technique. In LPS-treated human liver slices, NTCP mRNA was downregulated and showed an inverse correlation with the amounts of TNF-α and Il-1β produced. In contrast, MRP2 and BSEP mRNA levels were not affected under these conditions. However, after 24-h LPS challenge, both proteins were virtually absent in human liver slices, whereas marker proteins remained detectable. In conclusion, we show that posttranscriptional mechanisms play a more prominent role in LPS-induced regulation of human MRP2 and BSEP compared with the rat transporter proteins.

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