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Conference Paper: Oxidative stress induced by intermittent hypoxia exacerbates lipid accumulation and inflammation in a cell model of non-alcoholic steatohepatitis

TitleOxidative stress induced by intermittent hypoxia exacerbates lipid accumulation and inflammation in a cell model of non-alcoholic steatohepatitis
Authors
Issue Date2013
PublisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3
Citation
The 17th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine (ICSM), Hong Kong, China, 23 November 2013. In Journal of the Hong Kong College of Cardiology, 2013, v. 21 n. 2, p. 65, abstract no. OP3 How to Cite?
AbstractBackground/Aims: The prevalence of obstructive sleep apnea (OSA) is high in patients with non-alcoholic fatty liver disease (NAFLD) and NASH is a progressive hallmark of the pathogenesis of NAFLD. Chronic intermittent hypoxia is associated with recurrent episodes of oxygen desaturation and reoxygenation in OSA patients, leading to excessive production of reactive oxygen species (ROS). The causal link between OSA and NAFLD is not known and the mechanistic effect of intermittent hypoxia (IH) on the pathogenesis of NAFLD remains elusive. Here we tested the hypothesis that IH-induced oxidative stress aggravates lipid accumulation and inflammation induced by sodium palmitate in HepG2 cells. Materials and Methods: HepG2 cells were treated with sodium palmitate or vehicle under normoxia (Nx) or IH condition for 72 hours in the present or absence of a ROS scavenger MnTBAP. Cell viability was detected by MTT assay and intracellular lipid deposit was examined by oil red staining. Lipid peroxidation was measured by malondialdehyde (MDA) assay and levels of reactive oxygen species (ROS) were detected by CM-H2DCFDA staining. The expressions of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6), fatty acid uptake-associated genes (caveolin-1 and FATP5), fatty acid synthesis genes (SREBP1 and ACC1) and fatty acid β-oxidation gene ACOX were determined by real-time PCR. Results: Results showed that sodium palmitate increased lipid deposit in the cells and it also decreased cell viability. The effect of sodium palmitate was more prominent in the group co-treated with hypoxia. Levels of MDA and ROS and the expressions of IL-1β, TNF-α, IL-6 and caveolin-1, but not FATP5, were significantly increased in the palmitate- or hypoxia-treated group and were remarkably elevated in the co-treated group. These effects were abolished by MnTBAP treatment. In addition, levels of the expression of ACOX, SREBP1 and ACC1 were significantly lowered in the cells treated with palmitate or hypoxia and the expressions were much less in the cotreated group. Treatment of MnTBAP prevented the decreased expression of ACOX but had no effect on the SREBP1 and ACC1 expression. Conclusion: IH-induced oxidative stress exacerbates lipid accumulation and inflammation induced by sodium palmitate in HepG2 cells, probably mediated by an increase in lipid uptake and a decrease in the fatty acid β-oxidation.
DescriptionOral Presentation
Persistent Identifierhttp://hdl.handle.net/10722/203707
ISSN
2015 SCImago Journal Rankings: 0.102

 

DC FieldValueLanguage
dc.contributor.authorPan, Jen_US
dc.contributor.authorGuo, Ren_US
dc.contributor.authorLiong, ECen_US
dc.contributor.authorTipoe, GLen_US
dc.contributor.authorFung, MLen_US
dc.date.accessioned2014-09-19T16:11:28Z-
dc.date.available2014-09-19T16:11:28Z-
dc.date.issued2013en_US
dc.identifier.citationThe 17th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine (ICSM), Hong Kong, China, 23 November 2013. In Journal of the Hong Kong College of Cardiology, 2013, v. 21 n. 2, p. 65, abstract no. OP3en_US
dc.identifier.issn1027-7811-
dc.identifier.urihttp://hdl.handle.net/10722/203707-
dc.descriptionOral Presentation-
dc.description.abstractBackground/Aims: The prevalence of obstructive sleep apnea (OSA) is high in patients with non-alcoholic fatty liver disease (NAFLD) and NASH is a progressive hallmark of the pathogenesis of NAFLD. Chronic intermittent hypoxia is associated with recurrent episodes of oxygen desaturation and reoxygenation in OSA patients, leading to excessive production of reactive oxygen species (ROS). The causal link between OSA and NAFLD is not known and the mechanistic effect of intermittent hypoxia (IH) on the pathogenesis of NAFLD remains elusive. Here we tested the hypothesis that IH-induced oxidative stress aggravates lipid accumulation and inflammation induced by sodium palmitate in HepG2 cells. Materials and Methods: HepG2 cells were treated with sodium palmitate or vehicle under normoxia (Nx) or IH condition for 72 hours in the present or absence of a ROS scavenger MnTBAP. Cell viability was detected by MTT assay and intracellular lipid deposit was examined by oil red staining. Lipid peroxidation was measured by malondialdehyde (MDA) assay and levels of reactive oxygen species (ROS) were detected by CM-H2DCFDA staining. The expressions of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6), fatty acid uptake-associated genes (caveolin-1 and FATP5), fatty acid synthesis genes (SREBP1 and ACC1) and fatty acid β-oxidation gene ACOX were determined by real-time PCR. Results: Results showed that sodium palmitate increased lipid deposit in the cells and it also decreased cell viability. The effect of sodium palmitate was more prominent in the group co-treated with hypoxia. Levels of MDA and ROS and the expressions of IL-1β, TNF-α, IL-6 and caveolin-1, but not FATP5, were significantly increased in the palmitate- or hypoxia-treated group and were remarkably elevated in the co-treated group. These effects were abolished by MnTBAP treatment. In addition, levels of the expression of ACOX, SREBP1 and ACC1 were significantly lowered in the cells treated with palmitate or hypoxia and the expressions were much less in the cotreated group. Treatment of MnTBAP prevented the decreased expression of ACOX but had no effect on the SREBP1 and ACC1 expression. Conclusion: IH-induced oxidative stress exacerbates lipid accumulation and inflammation induced by sodium palmitate in HepG2 cells, probably mediated by an increase in lipid uptake and a decrease in the fatty acid β-oxidation.-
dc.languageengen_US
dc.publisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3-
dc.relation.ispartofJournal of the Hong Kong College of Cardiologyen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleOxidative stress induced by intermittent hypoxia exacerbates lipid accumulation and inflammation in a cell model of non-alcoholic steatohepatitisen_US
dc.typeConference_Paperen_US
dc.identifier.emailLiong, EC: eclionga@hkucc.hku.hken_US
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_US
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_US
dc.identifier.authorityTipoe, GL=rp00371en_US
dc.identifier.authorityFung, ML=rp00433en_US
dc.description.naturepublished_or_final_version-
dc.identifier.hkuros238123en_US
dc.identifier.volume21en_US
dc.identifier.issue2en_US
dc.identifier.spage65, abstract no. OP3-
dc.identifier.epage65, abstract no. OP3-
dc.publisher.placeHong Kong-

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