2015, Number 4
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Gac Med Mex 2015; 151 (4)
Cholesterol overload in hepatocytes affects nicotinamide adenine dinucleotide phosphate oxidase (NADPH) activity abrogating hepatocyte growth factor (HGF) induced cellular protection
López-Reyes AG, Martínez-Flores K, Clavijo-Cornejo D, Nuño-Lámbarri N, Palestino-Domínguez M, Souza V, Bucio L, Panduro A, Miranda RU, Gómez-Quiroz LE, Gutiérrez-Ruiz MC
Language: Spanish
References: 26
Page: 456-464
PDF size: 316.73 Kb.
ABSTRACT
The increment in the prevalence of obesity incidence in Mexico is leading to the increase in many chronic maladies, including
liver diseases. It is well known that lipid-induced liver sensitization is related to the kind of lipid rather than the amount of
them in the organ. Cholesterol overload in the liver aggravates the toxic effects of canonical liver insults. However, the status
on the repair and survival response elicited by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and the hepatocyte growth factor (HGF) is not completely understood. In the present, work we aimed to figure out the HGF/NADPH
oxidase-induced cellular protection in the hepatocyte with a cholesterol overload. Our results show that a hypercholesterolemic
diet induced liver damage and steatosis in mice. The hepatocytes isolated from these animals exhibited an increase in basal
NADPH oxidase activity, although transcriptional levels of some of its components were decreased. No effect on the oxidase
activity was observed in HGF treatments. The protective effect of HGF was abrogated as a result of cholesterol cellular
overload, calculated by a survival assay. In conclusion, the cholesterol overload in hepatocytes impairs the HGF/NADPH
oxidase-induced cellular protection.
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