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Expression of genes encoding mitochondrial proteins can distinguish nonalcoholic steatosis from steatohepatitis

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Bragoszewski P., Habior A., Walewska-Zielecka B., Ostrowski J.
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2007
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vol. 54
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issue 2
341-348
EN
In patients without substantial alcohol use, triglyceride accumulation in the liver can lead to nonalcoholic fatty liver disease (NAFLD) that may progress to nonalcoholic steatohepatitis (NASH). The differential diagnosis between NAFLD and NASH can be accomplished only by morphological examination. Although the relationship between mitochondrial dysfunction and the progression of liver pathologic changes has been described, the exact mechanisms initiating primary liver steatosis and its progression to NASH are unknown. We selected 16 genes encoding mitochondrial proteins which expression was compared by quantitative RT-PCR in liver tissue samples taken from patients with NAFLD and NASH. We found that 6 of the 16 examined genes were differentially expressed in NAFLD versus NASH patients. The expression of hepatic HK1, UCP2, ME2, and ME3 appeared to be higher in NASH than in NAFLD patients, whereas HMGCS2 and hnRNPK expression was lower in NASH patients. Although the severity of liver morphological injury in the spectrum of NAFLD-NASH may be defined at the molecular level, expression of these selected 6 genes cannot be used as a molecular marker aiding histological examination. Moreover, it is still unclear whether these differences in hepatic gene expression profiles truly reflect the progression of morphological abnormalities or rather indicate various metabolic and hormonal states in patients with different degrees of fatty liver disease.
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Macrophages, TGF-β1 expression and iron deposition in development of NASH

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Ananiev J., Penkova M., Tchernev G., Gulubova M.
Open Medicine
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2012
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vol. 7
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issue 5
599-603
EN
A wide range of molecular markers and different types of cells in liver are possible factors for progression of non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH) development of liver fibrosis. We investigated biopsies from 57 patients with NASH. The material was obtained from livers and was proceed immunohistochemistry antibodies against CD68 and TGF-beta 1. In addition, biopsies were evaluated for iron content. Macrophages/-positive/could be found in all 57 cases. The number of macrophages in the sinusoids correlated with the degree of portal fibrosis:64.% of the patients with mild or intensive fibrosis had high infiltration with CD68-positive cells, while 100% of the patients without fibrosis hadlow infiltration (χ2=8.56; p=0.003). In specimens we, 69.% of patients with different degree of fibrosis expressed TGF-β1 in their portal tracts, and 100% of patients without fibrosis did demonstrate expression of the protein (χ2=23.7; p<0.001). Hepatic iron was found in 100% (9) of patients with intensive fibrosis vs. 10.3% of the patients mild fibrosis (χ2=23.4; p<0.001). Our results suggest that the macrophages and macrophage-derived TGF-beta1 are the major factors responsible for development of fibrosis and progression of chronic liver disease.
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