PMID- 25586482
OWN - NLM
STAT- MEDLINE
DCOM- 20160223
LR  - 20181113
IS  - 1573-2576 (Electronic)
IS  - 0360-3997 (Linking)
VI  - 38
IP  - 3
DP  - 2015
TI  - Propofol Attenuates Lipopolysaccharide-Induced Monocyte Chemoattractant Protein-1 
      Production Through Enhancing apoM and foxa2 Expression in HepG2 Cells.
PG  - 1329-36
LID - 10.1007/s10753-014-0104-y [doi]
AB  - Monocyte chemoattractant protein-1 (MCP-1) is a cytokine that mediates the influx 
      of cells to sites of inflammation. Our group recently reported that propofol 
      exerted an anti-inflammatory effect and could inhibit lipopolysaccharide 
      (LPS)-induced production of pro-inflammatory cytokines. However, the effect and 
      possible mechanisms of propofol on MCP-1 expression remain unclear. 
      LPS-stimulated HepG2 cells were treated with 50 muM propofol for 0, 6, 12, and 24 
      h, respectively. The transcript and protein levels were measured by real-time 
      quantitative PCR and Western blot analyses, respectively. We found that propofol 
      markedly decreased both MCP-1 messenger RNA (mRNA) and protein levels in 
      LPS-stimulated HepG2 cells in a time-dependent manner. Expression of 
      apolipoprotein M (apoM) and forkhead box protein A2 (foxa2) was increased by 
      propofol treatment in HepG2 cells. In addition, the inhibitory effect of propofol 
      on MCP-1 expression was significantly abolished by small interfering RNA against 
      apoM and foxa2 in LPS-stimulated HepG2 cells. Propofol attenuates LPS-induced 
      MCP-1 production through enhancing apoM and foxa2 expression in HepG2 cells.
FAU - Ma, Xin
AU  - Ma X
AD  - Department of Anesthesiology, Nanfang Hospital, Southern Medical University, 
      Guangzhou, Guangdong, 510515, China.
FAU - Zhao, Jia-Yi
AU  - Zhao JY
FAU - Zhao, Zhen-Long
AU  - Zhao ZL
FAU - Ye, Jing
AU  - Ye J
FAU - Li, Shu-Fen
AU  - Li SF
FAU - Fang, Hai-Hong
AU  - Fang HH
FAU - Gu, Miao-Ning
AU  - Gu MN
FAU - Hu, Yan-Wei
AU  - Hu YW
FAU - Qin, Zai-Sheng
AU  - Qin ZS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (APOM protein, human)
RN  - 0 (Anesthetics, Intravenous)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Apolipoproteins)
RN  - 0 (Apolipoproteins M)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (FOXA2 protein, human)
RN  - 0 (Lipocalins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - 135845-92-0 (Hepatocyte Nuclear Factor 3-beta)
RN  - YI7VU623SF (Propofol)
SB  - IM
MH  - Anesthetics, Intravenous/*pharmacology
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Apolipoproteins/*biosynthesis/genetics
MH  - Apolipoproteins M
MH  - Cell Line
MH  - Cell Movement
MH  - Chemokine CCL2/*biosynthesis/genetics/metabolism
MH  - Hep G2 Cells
MH  - Hepatocyte Nuclear Factor 3-beta/*biosynthesis/genetics
MH  - Humans
MH  - Lipocalins/*biosynthesis/genetics
MH  - Lipopolysaccharides
MH  - Propofol/*pharmacology
MH  - RNA Interference
MH  - RNA, Messenger/biosynthesis
MH  - RNA, Small Interfering
EDAT- 2015/01/15 06:00
MHDA- 2016/02/26 06:00
CRDT- 2015/01/15 06:00
PHST- 2015/01/15 06:00 [entrez]
PHST- 2015/01/15 06:00 [pubmed]
PHST- 2016/02/26 06:00 [medline]
AID - 10.1007/s10753-014-0104-y [doi]
PST - ppublish
SO  - Inflammation. 2015;38(3):1329-36. doi: 10.1007/s10753-014-0104-y.