Skip Navigation

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow E-Letters: Submit a response to the article
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (13)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Nagata, T.
Right arrow Articles by Takahashi, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nagata, T.
Right arrow Articles by Takahashi, S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

British Journal of Anaesthesia, 2001, Vol. 86, No. 6 853-858
© 2001 The Board of Management and Trustees of the British Journal of Anaesthesia

Propofol inhibits FMLP-stimulated phosphorylation of p42 mitogen-activated protein kinase and chemotaxis in human neutrophils

T. Nagata, M. Kansha, K. Irita and S. Takahashi

Department of Anesthesiology and Critical Care Medicine, Kyushu University, Fukuoka, Japan*Corresponding author: 3-1-1 Maidashi, Higashi-ku, Fukuoka 812–8582, Japan

Propofol is used in the peri-operative setting and may affect some neutrophil functions. The effects of propofol on the function and intracellular signal transduction systems of neutrophils is controversial. Mitogen-activated protein kinase families (MAPKs) are members of the intracellular signal-transducing systems in eukaryotes. MAPKs have been shown to be involved in neutrophil chemotaxis by the use of PD98059, the specific inhibitor of MAPK/ERK kinase (MEK). The effects of propofol in dimethyl sulfoxide on phosphorylation of MAPKs and chemotaxis were investigated in human neutrophils. Isolated neutrophils (2x107 cells per ml) from healthy volunteers were incubated with propofol (2–500 µM) and stimulated by N-formyl-L-methionyl-phenylalanine (FMLP) (100 nM). The effects of propofol on the phosphorylation of p44/42 MAPK were investigated by immunoblotting. The effects of FMLP (1 µM) on chemotaxis were investigated with the under-agarose method. The phosphorylation of p42 MAPK and chemotaxis stimulated by FMLP were both inhibited by propofol at clinically relevant concentrations (>=10 and >=20 µM respectively). PD98059 (50 µM) also inhibited chemotaxis stimulated by FMLP, suggesting the involvement of p42 MAPK in the response. Propofol might therefore inhibit human neutrophil chemotaxis, at least in part, by suppressing the p44/42 MAPK pathway.

Br J Anaesth 2001; 86: 853–8


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 FASEB J.Home page
P. D. A. Issuree, P. N. Pushparaj, S. Pervaiz, and A. J. Melendez
Resveratrol attenuates C5a-induced inflammatory responses in vitro and in vivo by inhibiting phospholipase D and sphingosine kinase activities
FASEB J, August 1, 2009; 23(8): 2412 - 2424.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
G. Cohen, D. Ilic, J. Raupachova, and W. H. Horl
Resistin Inhibits Essential Functions of Polymorphonuclear Leukocytes
J. Immunol., September 15, 2008; 181(6): 3761 - 3768.
[Abstract] [Full Text] [PDF]

Home page
 Anesth. Analg.Home page
H. Wang, Z. Xue, Q. Wang, X. Feng, and Z. Shen
Propofol Protects Hepatic L02 Cells from Hydrogen Peroxide-Induced Apoptosis via Activation of Extracellular Signal-Regulated Kinases Pathway
Anesth. Analg., August 1, 2008; 107(2): 534 - 540.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
Z. T. Kneass and R. B. Marchase
Protein O-GlcNAc Modulates Motility-associated Signaling Intermediates in Neutrophils
J. Biol. Chem., April 15, 2005; 280(15): 14579 - 14585.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
W. C. Tsai, M. L. Rodriguez, K. S. Young, J. C. Deng, V. J. Thannickal, K. Tateda, M. B. Hershenson, and T. J. Standiford
Azithromycin Blocks Neutrophil Recruitment in Pseudomonas Endobronchial Infection
Am. J. Respir. Crit. Care Med., December 15, 2004; 170(12): 1331 - 1339.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
C. S. Hii, D. S. Anson, M. Costabile, V. Mukaro, K. Dunning, and A. Ferrante
Characterization of the MEK5-ERK5 Module in Human Neutrophils and Its Relationship to ERK1/ERK2 in the Chemotactic Response
J. Biol. Chem., November 26, 2004; 279(48): 49825 - 49834.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
N. Moghaddami, M. Costabile, P. K. Grover, H. P. A. Jersmann, Z. H. Huang, C. S. T. Hii, and A. Ferrante
Unique Effect of Arachidonic Acid on Human Neutrophil TNF Receptor Expression: Up-Regulation Involving Protein Kinase C, Extracellular Signal-Regulated Kinase, and Phospholipase A2
J. Immunol., September 1, 2003; 171(5): 2616 - 2624.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Pharmacol.Home page
M. Gouwy, S. Struyf, F. Mahieu, W. Put, P. Proost, and J. Van Damme
The Unique Property of the CC Chemokine Regakine-1 to Synergize with Other Plasma-Derived Inflammatory Mediators in Neutrophil Chemotaxis Does Not Reside in Its NH2-Terminal Structure
Mol. Pharmacol., July 1, 2002; 62(1): 173 - 180.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.