Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2005-6-20
pubmed:abstractText
Sepsis is a serious and life-threatening syndrome that often occurs in intensive care unit (ICU) patients. During sepsis, inflammatory cytokines and nitric oxide (NO) can be overproduced, causing tissue and cell injury. Propofol is an intravenous agent used for sedation of ICU patients. Our previous study showed that propofol has immunosuppressive effects on macrophage functions. This study was designed to evaluate the anti-inflammatory and antioxidative effects of propofol on the biosyntheses of tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta), IL-6, and NO in lipopolysaccharide (LPS)- activated macrophages. Exposure to a therapeutic concentration of propofol (50 microM), LPS (1 ng/mL), or a combination of these two drugs for 1, 6, and 24 h was not cytotoxic to the macrophages. ELISA revealed that LPS increased macrophage TNF-alpha, IL-1beta, and IL-6 protein levels in a time-dependent manner, whereas propofol significantly reduced the levels of LPS-enhanced TNF-alpha, IL-1beta, and IL-6 proteins. Data from RT-PCR showed that LPS induced TNF-alpha, IL-1beta, and IL-6 mRNA, but propofol inhibited these effects. LPS also increased NO production and inducible nitric oxide synthase (iNOS) expression in macrophages. Exposure of macrophages to propofol significantly inhibited the LPS-induced NO biosynthesis. The present study shows that propofol, at a therapeutic concentration, has anti-inflammatory and antioxidative effects on the biosyntheses of TNF-alpha, IL-1beta, IL-6, and NO in LPS-activated macro-phages and that the suppressive effects are exerted at the pretranslational level.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
1042
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
262-71
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15965071-Animals, pubmed-meshheading:15965071-Anti-Inflammatory Agents, pubmed-meshheading:15965071-Antioxidants, pubmed-meshheading:15965071-Cell Line, pubmed-meshheading:15965071-Cell Survival, pubmed-meshheading:15965071-Gene Expression Regulation, pubmed-meshheading:15965071-Inflammation, pubmed-meshheading:15965071-Interleukin-1, pubmed-meshheading:15965071-Interleukin-6, pubmed-meshheading:15965071-Lipopolysaccharides, pubmed-meshheading:15965071-Macrophages, pubmed-meshheading:15965071-Mice, pubmed-meshheading:15965071-Nitric Oxide Synthase Type II, pubmed-meshheading:15965071-Nitrites, pubmed-meshheading:15965071-Oxidation-Reduction, pubmed-meshheading:15965071-Propofol, pubmed-meshheading:15965071-RNA, Messenger, pubmed-meshheading:15965071-Tumor Necrosis Factor-alpha
pubmed:year
2005
pubmed:articleTitle
Anti-inflammatory and antioxidative effects of propofol on lipopolysaccharide-activated macrophages.
pubmed:affiliation
Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, No. 250, Wu-Hsing St., Taipei 110, Taiwan. rmchen@tmu.edu.tw
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't