TY - JOUR
T1 - Inhibitory effect of aspirin on cholera toxin-induced phospholipase and cyclo-oxygenase activity
AU - Liang, Yi fan
AU - Peterson, Johnny W.
AU - Reitmeyer, James C.
N1 - Funding Information:
This research was supported by the John Sealy Endowment Fund and research grant 2 ROI AI \[8401 from NIAID.
PY - 1990/10
Y1 - 1990/10
N2 - 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.
AB - 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.
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U2 - 10.1016/0378-1097(90)90360-3
DO - 10.1016/0378-1097(90)90360-3
M3 - Article
C2 - 2126514
AN - SCOPUS:0025133117
SN - 0378-1097
VL - 72
SP - 137
EP - 141
JO - FEMS Microbiology Letters
JF - FEMS Microbiology Letters
IS - 1-2
ER -