Papers

Peer-reviewed
Apr, 2016

Royal Jelly Constituents Increase the Expression of Extracellular Superoxide Dismutase through Histone Acetylation in Monocytic THP-1 Cells

JOURNAL OF NATURAL PRODUCTS
  • Junya Makino
  • ,
  • Rie Ogasawara
  • ,
  • Tetsuro Kamiya
  • ,
  • Hirokazu Hara
  • ,
  • Yukari Mitsugi
  • ,
  • Eiji Yamaguchi
  • ,
  • Akichika Itoh
  • ,
  • Tetsuo Adachi

Volume
79
Number
4
First page
1137
Last page
1143
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1021/acs.jnatprod.6b00037
Publisher
AMER CHEMICAL SOC

Extracellular superoxide dismutase (EC-SOD) is one of the main SOD isozymes and plays an important role in the prevention of cardiovascular diseases by accelerating the dismutation reaction of superoxide. Royal jelly includes 10-hydroxy-2-decenoic acid (10H2DA, 2), which regulates the expression of various types of genes in epigenetics through the effects of histone deacetylase (HDAC) antagonism. The expression of EC-SOD was previously reported to be regulated epigenetically through histone acetylation in THP-1 cells. Therefore, we herein evaluated the effects of the royal jelly constituents 10-hydroxydecanoic acid (10HDA, 1), sebacic acid (SA, 3), and 4-hydroperoxy-2-decenoic acid ethyl ester (4-HPO-DAEE, 4), which is a derivative of 2, on the expression of EC-SOD in THP-1 cells. The treatment with 1 mM 1, 2, or 3 or 100 mu M 4 increased EC-SOD expression and histone H3 and H4 acetylation levels. Moreover, the enrichment of acetylated histone H4 was observed in the proximal promoter region of EC-SOD and was caused by the partial promotion of ERK phosphorylation (only 4) and inhibition of HDAC activities, but not by the expression of HDACs. Overall, 4 exerted stronger effects than 1, 2, or 3 and has potential as a candidate or lead compound against atherosclerosis.

Link information
DOI
https://doi.org/10.1021/acs.jnatprod.6b00037
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/27049436
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000374915800058&DestApp=WOS_CPL
ID information
  • DOI : 10.1021/acs.jnatprod.6b00037
  • ISSN : 0163-3864
  • eISSN : 1520-6025
  • Pubmed ID : 27049436
  • Web of Science ID : WOS:000374915800058

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