PMID- 28182687
OWN - NLM
STAT- MEDLINE
DCOM- 20170828
LR  - 20190208
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 2
DP  - 2017
TI  - Lunasin attenuates obesity-related inflammation in RAW264.7 cells and 3T3-L1 
      adipocytes by inhibiting inflammatory cytokine production.
PG  - e0171969
LID - 10.1371/journal.pone.0171969 [doi]
LID - e0171969
AB  - Obesity has become a major threat to public health and is accompanied by chronic 
      low-grade inflammation, which leads to various pathological developments. 
      Lunasin, a natural seed peptide, exhibits several biological activities, such as 
      anti-carcinogenesis, anti-inflammatory, and antioxidant activities. However, the 
      mechanism of action of lunasin in obesity-related inflammation has not been 
      investigated. The aim of this study was to explore whether lunasin could reduce 
      the inflammation induced by obesity-related mediators in RAW264.7 cells and 
      3T3-L1 adipocytes and whether it could attenuate the crosstalk between the two 
      cell lines. RAW264.7 cells were cultured in leptin-containing medium, 
      adipocyte-conditioned medium (Ad-CM), or co-cultured with 3T3-L1 cells to mimic 
      the physiology of obesity. The data showed that the secretion of pro-inflammatory 
      cytokine interleukin-1beta (IL-1beta) was inhibited by lunasin after leptin activation 
      of RAW264.7 cells. In addition, lunasin decreased monocyte chemoattractant 
      protein-1 (MCP-1) and IL-1beta secretions in the Ad-CM model. Cytokine MCP-1, IL-6, 
      tumor necrosis factor (TNF)-alpha, and IL-1beta secretions were significantly decreased 
      by leptin or Ad-CM plus lipopolysaccharide stimulation. Subsequently, the 
      co-culture of the two cells refined the direct relation between them, resulting 
      in apparently increased MCP-1, and decreased IL-6 levels after lunasin treatment. 
      In 3T3-L1 adipocytes, lunasin also exhibited anti-inflammatory property by 
      inhibiting MCP-1, plasminogen activator inhibitor-1, and leptin productions 
      stimulated by (TNF)-alpha, lipopolysaccharide, or RAW264.7 cell-conditioned medium. 
      This result revealed that lunasin acts as a potential anti-inflammatory agent not 
      only in macrophages but also in adipocytes, disrupting the crosstalk between 
      these two cells. Therefore, this study suggests the intake of lunasin from diet 
      or as a supplement, for auxiliary prevention or therapy in obesity-related 
      inflammatory applications.
FAU - Hsieh, Chia-Chien
AU  - Hsieh CC
AUID- ORCID: 0000-0003-3993-0144
AD  - Department of Human Development and Family Studies, National Taiwan Normal 
      University, Taipei, Taiwan.
FAU - Chou, Mei-Jia
AU  - Chou MJ
AD  - Department of Human Development and Family Studies, National Taiwan Normal 
      University, Taipei, Taiwan.
FAU - Wang, Chih-Hsuan
AU  - Wang CH
AD  - Department of Human Development and Family Studies, National Taiwan Normal 
      University, Taipei, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20170209
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - 0 (Leptin)
RN  - 0 (Plant Proteins)
SB  - IM
MH  - 3T3 Cells
MH  - Adipocytes/cytology/*drug effects/metabolism
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Cell Differentiation
MH  - Cytokines/genetics/*metabolism
MH  - Leptin/genetics/metabolism
MH  - Mice
MH  - Obesity/*metabolism
MH  - Plant Proteins/*pharmacology
PMC - PMC5300240
COIS- The authors have declared that no competing interests exist.
EDAT- 2017/02/10 06:00
MHDA- 2017/08/29 06:00
PMCR- 2017/02/09
CRDT- 2017/02/10 06:00
PHST- 2016/09/21 00:00 [received]
PHST- 2017/01/27 00:00 [accepted]
PHST- 2017/02/10 06:00 [entrez]
PHST- 2017/02/10 06:00 [pubmed]
PHST- 2017/08/29 06:00 [medline]
PHST- 2017/02/09 00:00 [pmc-release]
AID - PONE-D-16-37846 [pii]
AID - 10.1371/journal.pone.0171969 [doi]
PST - epublish
SO  - PLoS One. 2017 Feb 9;12(2):e0171969. doi: 10.1371/journal.pone.0171969. 
      eCollection 2017.