Oligonol, a lychee fruit-derived low-molecular form of polyphenol mixture, suppresses inflammatory cytokine production from human monocytes

Monocytes produce high levels of inflammatory cytokines including IL-6 and TNF-α that are involved in autoimmunity, inflammatory diseases, cardiovascular disease and obesity. Therapies targeting IL-6 and TNF-α have been utilized in treating chronic inflammatory diseases. Oligonol is a lychee fruit-d...

Full description

Saved in:
Bibliographic Details
Published inHuman immunology Vol. 77; no. 6; pp. 512 - 515
Main Authors Lee, Naeun, Shin, Min Sun, Kang, Youna, Park, Kieyoung, Maeda, Takahiro, Nishioka, Hiroshi, Fujii, Hajime, Kang, Insoo
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.06.2016
Subjects
Online AccessGet full text
ISSN0198-8859
1879-1166
1879-1166
DOI10.1016/j.humimm.2016.04.011

Cover

More Information
Summary:Monocytes produce high levels of inflammatory cytokines including IL-6 and TNF-α that are involved in autoimmunity, inflammatory diseases, cardiovascular disease and obesity. Therapies targeting IL-6 and TNF-α have been utilized in treating chronic inflammatory diseases. Oligonol is a lychee fruit-derived low-molecular form of polyphenol mixture, typically catechin-type monomers and oligomers of proanthocyanidins, which are produced by an oligomerization process. Although previous studies reported anti-inflammatory properties of Oligonol, it is unknown whether and how Oligonol suppresses IL-6 and TNF-α production in human monocytes. The results of our study demonstrate that Oligonol (25μg/ml) decreases the production of IL-6 and TNF-α from human primary monocytes as measured by flow cytometry and ELISA. Such an anti-cytokine effect was likely mediated by the suppression of NF-κB activation without inducing cell death. Our findings raise the possibility of exploring the benefits of Oligonol in controlling inflammatory conditions, especially those associated with monocytes, in humans.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Equally contributed to this work.
ISSN:0198-8859
1879-1166
1879-1166
DOI:10.1016/j.humimm.2016.04.011