PMID- 25270720
OWN - NLM
STAT- MEDLINE
DCOM- 20150713
LR  - 20141114
IS  - 1532-2513 (Electronic)
IS  - 0892-3973 (Linking)
VI  - 36
IP  - 6
DP  - 2014 Dec
TI  - Atractylenolide I inhibits lipopolysaccharide-induced inflammatory responses via 
      mitogen-activated protein kinase pathways in RAW264.7 cells.
PG  - 420-5
LID - 10.3109/08923973.2014.968256 [doi]
AB  - Atractylenolide I (ATL-I) is a bioactive component of Rhizoma Atractylodis 
      macrocephalae. Although increasing evidence shows that ATL-I has an 
      anti-inflammatory effect, the anti-inflammatory molecular mechanism of ATL-I is 
      still unknown. In this study, we investigated the effect of ATL-I on cell 
      viability by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide 
      (MTT) assay and the level of interleukin-6 (IL-6) and tumor necrosis factor alpha 
      (TNF-alpha) by enzyme-linked immunosorbent assay (ELISA) in lipopolysaccharide 
      (LPS)-stimulated RAW264.7 cells. Further, we examined the effect of ATL-I on the 
      activation of nuclear factor-kappaB (NF-kappaB) and phosphorylation of extracellular 
      signal regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase 
      (p38) by Western blot. We also investigated the effect of ATL-I on the expression 
      of myeloid differentiation protein-2 (MD-2), CD14, complement receptor 3 (CR3), 
      scavenger receptor class A (SR-A), toll-like receptor 4 (TLR4) and myeloid 
      differentiation factor 88 (MyD88). We found that ATL-I showed no inhibitory 
      effect on cell viability at concentrations ranging from 1 microM to 100 microM and 
      markedly reduced the release of IL-6 and TNF-alpha at a concentrate-dependent manner. 
      In addition, ATL-I suppressed the activity of nuclear NF-kappaB and the 
      phosphorylation of ERK1/2 and p38 in LPS-treated RAW264.7 cells. Further analysis 
      showed that ATL-I inhibited the expression of MD-2, CD14, SR-A, TLR4 and MyD88, 
      but the expression of CR3 was unaffected. These data suggest that ATL-I shows an 
      anti-inflammatory effect by inhibiting TNF-alpha and IL-6 production. The 
      anti-inflammatory effects of ATL-I may be associated with the inhibition of the 
      NF-kappaB, ERK1/2 and p38 signaling pathways.
FAU - Ji, Guangquan
AU  - Ji G
AD  - College of Light Industry and Food Sciences, South China University of Technology 
      , Guangzhou , China and.
FAU - Chen, Renqiong
AU  - Chen R
FAU - Zheng, Jianxian
AU  - Zheng J
LA  - eng
PT  - Journal Article
DEP - 20141001
PL  - England
TA  - Immunopharmacol Immunotoxicol
JT  - Immunopharmacology and immunotoxicology
JID - 8800150
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Interleukin-6)
RN  - 0 (Lactones)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Sesquiterpenes)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (atractylenolide I)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Blotting, Western
MH  - Cell Culture Techniques
MH  - Cell Line
MH  - Cell Survival/drug effects
MH  - Interleukin-6/biosynthesis/immunology
MH  - Lactones/*pharmacology
MH  - Lipopolysaccharides/*pharmacology
MH  - MAP Kinase Signaling System/*drug effects
MH  - Macrophages/*drug effects/enzymology/*immunology
MH  - Mice
MH  - Sesquiterpenes/*pharmacology
MH  - Tumor Necrosis Factor-alpha/biosynthesis/immunology
OTO - NOTNLM
OT  - Atractylenolide I
OT  - MAPK
OT  - NF-kappaB
OT  - macrophage
OT  - tumor necrosis factor alpha
EDAT- 2014/10/02 06:00
MHDA- 2015/07/15 06:00
CRDT- 2014/10/02 06:00
PHST- 2014/10/02 06:00 [entrez]
PHST- 2014/10/02 06:00 [pubmed]
PHST- 2015/07/15 06:00 [medline]
AID - 10.3109/08923973.2014.968256 [doi]
PST - ppublish
SO  - Immunopharmacol Immunotoxicol. 2014 Dec;36(6):420-5. doi: 
      10.3109/08923973.2014.968256. Epub 2014 Oct 1.