PMID- 23262985
OWN - NLM
STAT- MEDLINE
DCOM- 20140502
LR  - 20211021
IS  - 1438-8359 (Electronic)
IS  - 0913-8668 (Linking)
VI  - 27
IP  - 3
DP  - 2013 Jun
TI  - Propofol attenuates lipopolysaccharide-induced monocyte chemoattractant protein-1 
      production through p38 MAPK and SAPK/JNK in alveolar epithelial cells.
PG  - 366-73
LID - 10.1007/s00540-012-1539-7 [doi]
AB  - PURPOSE: Propofol is widely used in sedation and surgical procedures involving 
      patients with acute lung injury (ALI), a common complication in critically ill 
      patients. Monocyte chemoattractant protein-1 (MCP-1) plays an important role in 
      pathological changes in ALI. The present study investigated the anti-inflammatory 
      effect and mechanism of propofol on MCP-1 production and mitogen-activated 
      protein kinase (MAPK) phosphorylation induced by lipopolysaccharide (LPS) in 
      alveolar epithelial cells (AECs). METHODS: AECs were treated with 1 mug/ml LPS for 
      30 min, 1 h, 6 h, or 24 h following pretreatment with 12.5-100 muM propofol for 
      30 min. Cytokines and chemokines secretion were profiled using cytokine array, 
      and mRNA and protein levels of MCP-1 were measured by RT-PCR and ELISA. The 
      phosphorylation of p38 MAPK, p44/42 MAPK, SAPK/JNK, ATF-2, and c-Jun were 
      measured by Western blot analysis. RESULTS: Propofol at 50 and 100 muM 
      dose-dependently inhibited MCP-1 mRNA expression (P < 0.05), and also propofol at 
      50 muM decreased extracellular MCP-1 protein levels (P < 0.05) compared to the LPS 
      group. Propofol at 12.5-50 muM inhibited LPS-induced phosphorylation of p38 MAPK, 
      p44/42 MAPK, SAPK/JNK, ATF-2, and c-Jun in AECs. CONCLUSIONS: Propofol at 
      clinically relevant concentrations attenuated LPS-induced MCP-1 mRNA expression 
      and secretion by inhibiting the phosphorylation of p38 MAPK, SAPK/JNK, ATF-2, and 
      c-Jun exerting its anti-inflammatory effects in AECs. These results suggest that 
      propofol may modulate inflammatory response at clinically achievable 
      concentrations in ALI.
FAU - Wei, Liguo
AU  - Wei L
AD  - Department of Anesthesiology, Nihon University School of Dentistry at Matsudo, 
      2-870-1 Sakaecho-Nishi, Matsudo, Chiba, Japan. wlg5616854@msn.cn
FAU - Matsumoto, Hiroko
AU  - Matsumoto H
FAU - Yamaguchi, Hidenori
AU  - Yamaguchi H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121221
PL  - Japan
TA  - J Anesth
JT  - Journal of anesthesia
JID - 8905667
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - EC 2.7.12.2 (MAP Kinase Kinase 4)
RN  - YI7VU623SF (Propofol)
SB  - IM
MH  - Animals
MH  - Cell Line, Tumor
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Cytokines/genetics/metabolism
MH  - Drug Interactions
MH  - Epithelial Cells/*drug effects/enzymology/metabolism
MH  - Female
MH  - Humans
MH  - Lipopolysaccharides/antagonists & inhibitors/*pharmacology
MH  - MAP Kinase Kinase 4/genetics/metabolism
MH  - Phosphorylation/drug effects
MH  - Propofol/*pharmacology
MH  - Pulmonary Alveoli/*drug effects/enzymology/metabolism
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - p38 Mitogen-Activated Protein Kinases/genetics/*metabolism
EDAT- 2012/12/25 06:00
MHDA- 2014/05/03 06:00
CRDT- 2012/12/25 06:00
PHST- 2012/08/26 00:00 [received]
PHST- 2012/11/29 00:00 [accepted]
PHST- 2012/12/25 06:00 [entrez]
PHST- 2012/12/25 06:00 [pubmed]
PHST- 2014/05/03 06:00 [medline]
AID - 10.1007/s00540-012-1539-7 [doi]
PST - ppublish
SO  - J Anesth. 2013 Jun;27(3):366-73. doi: 10.1007/s00540-012-1539-7. Epub 2012 Dec 
      21.