Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김영미 | - |
dc.date.accessioned | 2019-04-15T06:18:47Z | - |
dc.date.available | 2019-04-15T06:18:47Z | - |
dc.date.issued | 2015-11 | - |
dc.identifier.citation | PHARMAZIE, v. 70, No. 11, Page. 733-739 | en_US |
dc.identifier.issn | 0031-7144 | - |
dc.identifier.uri | https://www.ingentaconnect.com/contentone/govi/pharmaz/2015/00000070/00000011/art00007 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/101939 | - |
dc.description.abstract | Nonalcoholic fatty liver disease is recognized as the most commonly occurring chronic liver disease. Liver X receptor alpha (LXR alpha) and sterol regulatory element-binding protein (SREBP)-1c play a central role in de novo fatty acid synthesis. This study investigated pharmacological effects of nectandrin B, a lignan isolated from nutmeg extract, on hepatic lipogenesis stimulated by LXR alpha -SREBP-1c-mediated pathway and the possible molecular basis. The reporter gene assay revealed that nectandrin B completely represses LXR alpha activity enhanced by a synthetic LXR alpha ligand (T0901317) in HepG2 cells. The inhibitory effect was further supported by the suppression of mRNA expression of LXR alpha target genes, SREBP-1c and LXR alpha itself. Nectandrin B also inhibited the increase in SREBP-1c expression promoted by insulin plus high glucose, major contributors to hepatic lipid accumulation. LXR alpha -SREBP-1c-mediated induction of acetylCoA carboxylase 1 and fatty acid synthase, major genes for de novo lipogenesis, was suppressed by nectandrin B. Moreover, Oil Red O staining showed that nectandrin B notably attenuates LXR alpha-induced lipid accumulation. AMP-activated protein kinase (AMPK) inhibits the activities of LXR alpha and SREBP-1c. Nectandrin B strongly activated AMPK signaling in HepG2 cells. Taken together, the suppressive effects of nectandrin B on lipogenic gene expression and lipid accumulation in hepatocytes may be due to its inhibitory effect on the LXR alpha-SREBP-1c pathway presumably via AMPK activation. These results suggest the potential of nectandrin B as a therapeutic candidate for fatty liver disease. | en_US |
dc.description.sponsorship | This work was supported by the Research Fund of Hanyang University (HY-2013-N). | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | GOVI-VERLAG PHARMAZEUTISCHER VERLAG GMBH | en_US |
dc.subject | ELEMENT-BINDING PROTEIN-1C | en_US |
dc.subject | MYRISTICA-FRAGRANS NUTMEG | en_US |
dc.subject | ENDOTHELIAL-CELLS ROLE | en_US |
dc.subject | FATTY LIVER | en_US |
dc.subject | METABOLIC SYNDROME | en_US |
dc.subject | MOUSE-LIVER | en_US |
dc.subject | EXPRESSION | en_US |
dc.subject | PATHWAY | en_US |
dc.subject | STEATOSIS | en_US |
dc.subject | SREBP-1C | en_US |
dc.title | Nectandrin B, a lignan isolated from nutmeg, inhibits liver X receptor-alpha-induced hepatic lipogenesis through AMP-activated protein kinase activation | en_US |
dc.type | Article | en_US |
dc.relation.no | 11 | - |
dc.relation.volume | 70 | - |
dc.identifier.doi | 10.1691/ph.2015.5661 | - |
dc.relation.page | 733-739 | - |
dc.relation.journal | PHARMAZIE | - |
dc.contributor.googleauthor | Choi, Du Gon | - |
dc.contributor.googleauthor | Kim, Eun Kyung | - |
dc.contributor.googleauthor | Yang, Jin Won | - |
dc.contributor.googleauthor | Song, Jae Sook | - |
dc.contributor.googleauthor | Kim, Young Mi | - |
dc.relation.code | 2015002428 | - |
dc.sector.campus | E | - |
dc.sector.daehak | COLLEGE OF PHARMACY[E] | - |
dc.sector.department | DEPARTMENT OF PHARMACY | - |
dc.identifier.pid | ymikim12 | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.