Abstract
When L-platelet-activating factor (PAF) or alprazolam (a PAF antagonist) was administered to lipopolysaccharide (LPS)-treated mice, the level of plasma tumor necrosis factor (TNFα) determined by either ELISA or a cytotoxic assay using WEHI cells was significantly lowered. The inactive stereoisomer, D-PAF, was not effective in lowering plasma TNFα levels in LPS-treated mice. The decrease in plasma TNFα induced by L-PAF or alprazolam was partly reversed by indomethacin. Despite a decrease in plasma TNFα, L-PAF or alprazolam caused an increase in the amount of TNFα mRNA present in the kidneys and the livers of LPS-treated mice, suggesting that a posttranscriptional event leading to the synthesis or release of TNFα was inhibited by these agents.
Original language | English (US) |
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Pages (from-to) | 1081-1086 |
Number of pages | 6 |
Journal | Journal of Infectious Diseases |
Volume | 162 |
Issue number | 5 |
DOIs | |
State | Published - Nov 1990 |
Externally published | Yes |
ASJC Scopus subject areas
- General Medicine