PMID- 25876063
OWN - NLM
STAT- MEDLINE
DCOM- 20160609
LR  - 20161125
IS  - 1557-7600 (Electronic)
IS  - 1096-620X (Linking)
VI  - 18
IP  - 9
DP  - 2015 Sep
TI  - Osthole Attenuates Inflammatory Responses and Regulates the Expression of 
      Inflammatory Mediators in HepG2 Cells Grown in Differentiated Medium from 3T3-L1 
      Preadipocytes.
PG  - 972-9
LID - 10.1089/jmf.2014.3314 [doi]
AB  - This study explored the anti-inflammatory mechanisms by which osthole acted on 
      HepG2 cells cultured in a differentiated medium from cultured 3T3-L1 preadipocyte 
      cells. HepG2 cells, a human liver cell line, were treated with various 
      concentrations of osthole in differentiated media from cultured 3T3-L1 cells to 
      evaluate proinflammatory cytokines, inflammatory mediators, and signaling 
      pathways. We used enzyme-linked immunosorbent assay kits to determine the levels 
      of proinflammatory cytokines, real-time polymerase chain reaction to assay the 
      mRNA expression, and western blot to determine the expression of cyclooxygenase-2 
      (COX-2) and heme oxygenase-1 (HO-1) proteins. We also investigated inflammatory 
      mechanism pathway members, including mitogen-activated protein kinase (MAPK) and 
      nuclear transcription factor kappa-B (NF-kappaB). Osthole was able to suppress the 
      levels of proinflammatory cytokines interleukin (IL)-1beta and IL-6, as well as 
      chemokines monocyte chemoattractant protein-1 and IL-8. In addition, COX-2 was 
      suppressed and HO-1 expression was increased in a concentration-dependent manner. 
      Osthole was also able to decrease IkappaB-alpha phosphorylation and suppress the 
      phosphorylation of MAPKs. These results suggest that osthole has 
      anti-inflammatory effects as demonstrated by the decreased proinflammatory 
      cytokine and mediator production through suppression of the NF-kappaB and MAPK 
      signaling pathways in HepG2 cells when they are incubated on the differentiated 
      medium from 3T3-L1 cells.
FAU - Wu, Shu-Ju
AU  - Wu SJ
AD  - 1 Department of Nutrition and Health Sciences, Chang Gung University of Science 
      and Technology , Tao-Yuan, Taiwan .
AD  - 2 Research Center for Industry of Human Ecology, Chang Gung University of Science 
      and Technology , Tao-Yuan, Taiwan .
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150415
PL  - United States
TA  - J Med Food
JT  - Journal of medicinal food
JID - 9812512
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Coumarins)
RN  - 0 (Cytokines)
RN  - 0 (I-kappa B Proteins)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukins)
RN  - 0 (NF-kappa B)
RN  - 0 (NFKBIA protein, human)
RN  - 0 (Nfkbia protein, mouse)
RN  - 0 (Plant Extracts)
RN  - 139874-52-5 (NF-KappaB Inhibitor alpha)
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - XH1TI1759C (osthol)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipocytes/metabolism
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology/therapeutic use
MH  - Apiaceae/*chemistry
MH  - Coumarins/pharmacology/*therapeutic use
MH  - Cyclooxygenase 2/metabolism
MH  - Cytokines/metabolism
MH  - Heme Oxygenase-1/metabolism
MH  - Hep G2 Cells
MH  - Humans
MH  - I-kappa B Proteins/metabolism
MH  - Inflammation/drug therapy/*metabolism
MH  - Inflammation Mediators/*metabolism
MH  - Interleukins/metabolism
MH  - MAP Kinase Signaling System/drug effects
MH  - Mice
MH  - NF-KappaB Inhibitor alpha
MH  - NF-kappa B/metabolism
MH  - *Phytotherapy
MH  - Plant Extracts/*pharmacology/therapeutic use
MH  - Signal Transduction
OTO - NOTNLM
OT  - HepG2
OT  - MAPK
OT  - NF-kappaB
OT  - inflammation
OT  - osthole
EDAT- 2015/04/16 06:00
MHDA- 2016/06/10 06:00
CRDT- 2015/04/16 06:00
PHST- 2015/04/16 06:00 [entrez]
PHST- 2015/04/16 06:00 [pubmed]
PHST- 2016/06/10 06:00 [medline]
AID - 10.1089/jmf.2014.3314 [doi]
PST - ppublish
SO  - J Med Food. 2015 Sep;18(9):972-9. doi: 10.1089/jmf.2014.3314. Epub 2015 Apr 15.