Evaluation of nitrite/nitrate levels in relation to oxidative stress parameters in liver cirrhosis

Ergün, Yusuf; Kurutaş, Ergül Belge; Özdil, Burhan; Güneşaçar, Ramazan; Ergün, Yılmaz

doi:10.1016/j.clinre.2010.12.009

Cited by 15 publications

(11 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…13,28 Our work also elucidated the role of cholesterol and NO in MMP-9 induction in an in vitro model of HSC-T6 cells. As shown in Figure 7a, MMP-9 expression was significantly increased in HSC-T6 cells incubated with cholesterol.…”

Section: Effects Of Pharmacological Inhibition Of Inos In Hcd-inducedmentioning

confidence: 82%

“…Data from animal models of fibrosis or NASH-related liver fibrosis have shown conflicting results of both beneficial and deleterious effects of iNOS. [12][13][14][15][16][17][18][19] The exact reason/s for these paradoxical effects is difficult to explain. Therefore, the present study was undertaken to elucidate the role of iNOS in the pathophysiology of liver fibrosis due to consumption of a HCD.…”

mentioning

confidence: 99%

See 1 more Smart Citation

The role of iNOS in cholesterol-induced liver fibrosis

Anavi

Eisenberg-Bord

Hahn-Obercyger

et al. 2015

Laboratory Investigation

View full text Add to dashboard Cite

Accumulation of cholesterol in the liver is associated with the development of non-alcoholic steatohepatitis-related fibrosis. However, underlying mechanisms are not well understood. The present study investigated the role of inducible nitric oxide synthase (iNOS) in cholesterol-induced liver fibrosis by feeding wild-type (WT) and iNOS-deficient mice with control or high-cholesterol diet (HCD) for 6 weeks. WT mice fed with HCD developed greater liver fibrosis, compared with iNOS-deficient mice, as evident by Sirius red staining and higher expression levels of profibrotic genes. Enhanced liver fibrosis in the presence of iNOS was associated with hypoxia-inducible factor-1a stabilization, matrix metalloproteinase-9 expression, and enhanced hepatic DNA damage. The profibrotic role of iNOS was also demonstrated in vivo using a selective inhibitor of iNOS as well as in vitro in a rat liver stellate cell line (HSC-T6). In conclusion, these findings suggest that iNOS is an important mediator in HCD-induced liver fibrosis.Laboratory Investigation (2015) 95, 914-924;

show abstract

Section: Effects Of Pharmacological Inhibition Of Inos In Hcd-inducedmentioning

confidence: 82%

mentioning

confidence: 99%

The role of iNOS in cholesterol-induced liver fibrosis

Anavi

Eisenberg-Bord

Hahn-Obercyger

et al. 2015

Laboratory Investigation

View full text Add to dashboard Cite

show abstract

“…The nitrite levels were determined in homogenates of liver of mice as an indicator of NO production [23]. Samples dissolved in phosphate buffer and centrifuged at 2000 g for 20 minutes.…”

Section: Estimate Of Nitrite Oxidementioning

confidence: 99%

Beneficial effects of Androctonus australis hector venom and its non-toxic fraction in the restoration of early hepatocyte-carcinogenesis induced by FB1 mycotoxin: Involvement of oxidative biomarkers

Bekkari

Laraba-Djebari

2015

Experimental and Molecular Pathology

View full text Add to dashboard Cite

“…Kupffer cells, the resident macrophages of the liver, have been demonstrated to decisively mediate wound-related hepatic inflammation, and consequently initiate liver fibrosis 1, 6, 7. In response to liver damage agents, including harmful use of alcohol, hepatitis C virus infection (HCV) and non-alcoholic steatohepatitis, Kupffer cells are activated starting to express proinflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin (IL) 1β and IL-6, several chemoattractant molecules as it is the case for monocyte chemotactic protein 1 (MCP-1) and CXCL8 8, and some enzymes, such as the inducible nitric oxide synthase (iNOS) 9. Consequently, additional immune cells are recruited into the liver that shows active infiltration of CD4 + and CD8 + T lymphocytes, natural killer cells, and neutrophils associated with high levels of interferon-gamma (IFN-γ) and IL-12 5-10.…”

Section: Introductionmentioning

confidence: 99%

Th2-Associated Alternative Kupffer Cell Activation Promotes Liver Fibrosis without Inducing Local Inflammation

et al. 2011

View full text Add to dashboard Cite

Cirrhosis is the final outcome of liver fibrosis. Kupffer cell-mediated hepatic inflammation is considered to aggravate liver injury and fibrosis. Alternatively-activated macrophages are able to control chronic inflammatory events and trigger wound healing processes. Nevertheless, the role of alternative Kupffer cell activation in liver harm is largely unclear. Thus, we evaluated the participation of alternatively-activated Kupffer cells during liver inflammation and fibrosis in the murine model of carbon tetrachloride-induced hepatic damage. To stimulate alternative activation in Kupffer cells, 20 Taenia crassiceps (Tc) larvae were inoculated into BALBc/AnN female mice. Six weeks post-inoculation, carbon tetrachloride or olive oil were orally administered to Tc-inoculated and non-inoculated mice twice per week during other six weeks. The initial exposure of animals to T. crassiceps resulted in high serum concentrations of IL-4 accompanied by a significant increase in the hepatic mRNA levels of Ym-1, with no alteration in iNOS expression. In response to carbon tetrachloride, recruitment of inflammatory cell populations into the hepatic parenchyma was 5-fold higher in non-inoculated animals than Tc-inoculated mice. In contrast, carbon tetrachloride-induced liver fibrosis was significantly less in non-inoculated animals than in the Tc-inoculated group. The latter showed elevated IL-4 serum levels and low IFN-γ concentrations during the whole experiment, associated with hepatic expression of IL-4, TGF-β, desmin and α-sma, as well as increased mRNA levels of Arg-1, Ym-1, FIZZ-1 and MMR in Kupffer cells. These results suggest that alternative Kupffer cell activation is favored in a Th2 microenvironment, whereby such liver resident macrophages could exhibit a dichotomic role during chronic hepatic damage, being involved in attenuation of the inflammatory response but at the same time exacerbation of liver fibrosis.

show abstract

Evaluation of nitrite/nitrate levels in relation to oxidative stress parameters in liver cirrhosis

Cited by 15 publications

References 32 publications

The role of iNOS in cholesterol-induced liver fibrosis

The role of iNOS in cholesterol-induced liver fibrosis

Beneficial effects of Androctonus australis hector venom and its non-toxic fraction in the restoration of early hepatocyte-carcinogenesis induced by FB1 mycotoxin: Involvement of oxidative biomarkers

Th2-Associated Alternative Kupffer Cell Activation Promotes Liver Fibrosis without Inducing Local Inflammation

Contact Info

Product

Resources

About