Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/80594
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dc.contributorDepartment of Applied Biology and Chemical Technologyen_US
dc.creatorLi, XXen_US
dc.creatorLu, XYen_US
dc.creatorZhang, SJen_US
dc.creatorChiu, APen_US
dc.creatorLo, LHen_US
dc.creatorLargaespada, DAen_US
dc.creatorChen, QBen_US
dc.creatorKeng, VWen_US
dc.date.accessioned2019-04-23T08:16:20Z-
dc.date.available2019-04-23T08:16:20Z-
dc.identifier.urihttp://hdl.handle.net/10397/80594-
dc.language.isoenen_US
dc.publisherElsevier Massonen_US
dc.rights© 2018 The Authors. Published by Elsevier Masson SAS. This is an open access article under the CC BY license (http://creativecommons.org/licenses/BY/4.0/).en_US
dc.rightsThe following publication: Li, X. X., Lu, X. Y., Zhang, S. J., Chiu, A. P., Lo, L. H., Largaespada, D. A., ... & Keng, V. W. (2019). Sodium tanshinone IIA sulfonate ameliorates hepatic steatosis by inhibiting lipogenesis and inflammation. Biomedicine & Pharmacotherapy, 111, 68-75 is available at https://doi.org/10.1016/j.biopha.2018.12.019en_US
dc.subjectNAFLDen_US
dc.subjectPRKAA1en_US
dc.subjectSIRT1en_US
dc.subjectSodium tanshinone IIA sulfonateen_US
dc.titleSodium tanshinone IIA sulfonate ameliorates hepatic steatosis by inhibiting lipogenesis and inflammationen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage68en_US
dc.identifier.epage75en_US
dc.identifier.volume111en_US
dc.identifier.doi10.1016/j.biopha.2018.12.019en_US
dcterms.abstractNon-alcoholic fatty liver disease (NAFLD) is becoming an epidemic disease in adults and children worldwide. Importantly, there are currently no approved treatments available for NAFLD. This study aims to investigate the potential applications of sodium tanshinone IIA sulfonate (STS) on improving the NAFLD condition using both in vitro and in vivo approaches. The results showed that STS markedly inhibited lipid accumulation in oleic acid (OA) and palmitic acid (PA) treated HepG2 and primary immortalized human hepatic (PIH) cells. STS suppressed lipogenesis by inhibiting expression of sterol regulatory element binding transcription factor 1 (SREBF1), fatty acid synthase (FASN) and stearoyl-CoA desaturase (SCD). In addition, STS reduced inflammation in cells treated with OA-PA, shown by decreased transcriptional levels of tumor necrosis factor (TNF), transforming growth factor beta 1 (TGFB1) and interleukin 1 beta (IL1B). Consistently, protective effects on hepatic steatosis in db/db mice were observed after STS administration, demonstrated by decreased lipid accumulation in mouse hepatocytes. This protective effect might be associated with STS induced activation of sirtuin 1 (SIRT1)/protein kinase AMP-activated catalytic subunit alpha 1 (PRKAA1) pathways. Our findings suggest a potential therapeutic role for STS in the treatment of NAFLD.en_US
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationBiomedicine and pharmacotherapy, Mar. 2019, v. 111, p. 68-75en_US
dcterms.isPartOfBiomedicine and pharmacotherapyen_US
dcterms.issued2019-03-
dc.identifier.scopus2-s2.0-85058556037-
dc.identifier.eissn0753-3322en_US
dc.description.validate201904 bcmaen_US
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumbera0613-n02-
dc.identifier.SubFormID593-
dc.description.fundingSourceRGCen_US
dc.description.fundingTextC5012-15Een_US
dc.description.pubStatusPublisheden_US
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