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prostaglandin/cannabis
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Cannabinoids stimulate prostaglandin production by human gestational tissues through a tissue- and CB1-receptor-specific mechanism.
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Endocannabinoids have been implicated in the mechanisms of implantation, maintenance of pregnancy, and parturition in women. Intrauterine prostaglandin production and actions are also critical in each of these mechanisms. Hence, we have evaluated the effects of cannabinoids on prostaglandin
Prostaglandin synthesis inhibitors reduce Cannabis and restraint stress induced increase in rat brain serotonin concentrations.
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Cannabis resin (CI) produced a dose-related increase in rat brain serotonin concentrations, whereas restraint stress produced maximal rise of the neurotransmitter concentrations at 1 h, followed by a tendency to normalise by 4 h. The prostaglandin (PG) synthesis inhibitors, diclofenac and
Prostaglandins and cannabis. XII. The effect of cannabinoid structure on the synthesis of prostaglandins by human lung fibroblasts.
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Earlier findings indicated that several other cannabinoids in addition to delta 1-tetrahydro-cannabinol (THC) were able to stimulate the synthesis of prostaglandins in cell culture systems. The present study was initiated to delineate the structural requirements for this effect within the
Decrease in prostaglandin level is a prerequisite for the expression of cannabinoid withdrawal: a quasi abstinence approach.
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Cannabinoid withdrawal has been indicated in both human and animal subjects. One of pathways proposed to facilitate cannabinoid action is the arachidonic acid cascade. Previously, we have shown that prostaglandin attenuated the expression of withdrawal signs in tetrahydrocannabinol-dependent mice.
Prostaglandins and cannabis XV. Comparison of enantiomeric cannabinoids in stimulating prostaglandin synthesis in fibroblasts.
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Stereospecificity has been reported for a number of actions of the cannabinoids in a variety of systems. In the present report, we have shown that this effect can also be demonstrated when human lung fibroblasts in monolayer culture are stimulated by cannabinoids to produce prostaglandin E2 (PGE2).
Prostaglandins and cannabis XIV. Tolerance to the stimulatory actions of cannabinoids on arachidonate metabolism.
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The stimulation of prostaglandin E2 synthesis by delta 1-tetrahydrocannabinol in cultured cells is rapidly diminished by successive exposures to the drug at 24-hr intervals. Cannabidiol and cannabicyclol, two other constituents of cannabis, also displayed this in vitro tolerance effect. The
Possible role of prostaglandins in the effects of the cannabinoids on adenylate cyclase activity.
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In vitro, the cannabinoids delta 9-tetrahydrocannabinol (delta 9-THC), 11-OH-delta 9-THC, cannabidiol and cannabinol all increased adenylate cyclase activity in mouse cerebral cortical homogenates. Levonantradol, a synthetic cannabinoid analog, also increased adenylate cyclase activity while its
Prostaglandins and cannabis--IX. Stimulation of prostaglandin E2 synthesis in human lung fibroblasts by delta 1-tetrahydrocannabinol.
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Preliminary data [S. Burstein and S. A. Hunter, Biochem. Pharmac. 27, 1275 (1978)] showed that cannabinoids at levels of 1 microM or greater elevated the concentrations of prostaglandins in cell culture models. Further study [S. Burstein and S. A. Hunter, J. clin. Pharmac. 21, 240S (1981)] led to
Cannabinoids and pain responses: a possible role for prostaglandins.
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The principal metabolite of delta 1-THC, delta 1-THC-7-oic acid exhibits significant analgesic action in the mouse hot plate test. The parent delta 1-THC has a similar effect when measured at later time points; however, 10 min after drug administration, a pronounced hyperalgesia is seen. This
Prostaglandins and cannabis--XVI. Antagonism of delta 1-tetrahydrocannabinol action by its metabolites.
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Prior exposure of cells in vitro to delta 1-tetrahydrocannabinol-7-oic acid (delta 1-THC-7-oic acid) reduced the degree of stimulation of prostaglandin synthesis incurred by subsequent treatment with delta 1-THC. The site of action of this inhibitory effect seemed to be on cyclooxygenase and not at
Prostaglandins and cannabis--VIII. Elevation of phospholipase A2 activity by cannabinoids in whole cells and subcellular preparations.
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The previously reported release of arachidonic acid by THC has now been demonstrated in murine Leydig cells and WI-38 human lung fibroblasts showing the generality of the effect. The release reaction could be antagonized by phospholipase A2 inhibitors such as quinacrine and quinine, suggesting that
Isolation from Cannabis sativa L. of cannflavin--a novel inhibitor of prostaglandin production.
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The isolation from Cannabis sativa L. of an inhibitor of prostaglandin (PG) E2 production by cultured rheumatoid synovial cells is described. This agent, for which the name Cannflavin has been coined, is distinct from cannabinoids on the basis of isolation procedure, preliminary structural analysis
Lipids and addiction: how sex steroids, prostaglandins, and cannabinoids interact with drugs of abuse.
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Lipidomics aims to identify and characterize all endogenous species of lipids and understand their roles in cellular signaling and, ultimately, the functioning of the organism. We are on the cusp of fully understanding the functions of many of the lipid signaling systems that have been identified
Investigation of structural analogs of prostaglandin amides for binding to and activation of CB1 and CB2 cannabinoid receptors in rat brain and human tonsils.
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Prostaglandins and cannabis. II. Inhibition of biosynthesis by the naturally occurring cannabinoids.
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