Inhibitory effect of aspirin on cholera toxin-induced phospholipase and cyclo-oxygenase activity

Yi fan Liang, Johnny W. Peterson, James C. Reitmeyer

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

Cholera toxin (CT) stimulated phospholipase activity and caused [3H]arachidonic acid (3H-AA) release in a murine macrophage/monocyte cell line. Pretreatment of cells with dexamethasone, a phospholipase A2 (PLA2) inhibitor, did not affect CT-induced 3H-AA release. In contrast, aspirin, which is an inhibitor of phospholipase C (PLC), blocked CT-induced 3H-AA release and subsequent prostaglandin (PC) synthesis. The inhibitory effect of aspirin was dose dependent, with 4 mM reducing the CT response by approximately 50%. Similarly, inhibition was time dependent, occurring when the drug was added to the culture medium as late as 30 min after CT. Brief exposure (30 min) of the cells to aspirin did not alter their subsequent response to CT, but 3H-AA release from cells exposed to aspirin for 2.5 h was irreversibly inhibited. The data suggested that CT stimulation of AA metabolism may involved increased PLC activity.

Original languageEnglish (US)
Pages (from-to)137-141
Number of pages5
JournalFEMS Microbiology Letters
Volume72
Issue number1-2
DOIs
StatePublished - Oct 1990

ASJC Scopus subject areas

  • Microbiology
  • Molecular Biology
  • Genetics

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