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Cannabinoids Impair the Formation of Cholesteryl Ester in Cultured Human Cells

Cannabinoids Impair the Formation of Cholesteryl Ester in Cultured Human Cells The ability of cultured human fibroblasts to form cholesteryl esters from 14C-oleate Is impalred by A'-tetrahydrocannabinol, cannabidiol, and cannabinol, a group of natural products isolated from Cannabls satlwa. This inhibition is compound and dose-related; 30 μM cannabidiol reduced esterlficatlon to less than 20' of the control values. The esteriflcation of endogenous and exogenous cholesterol was affected, since lnhlbition was seen with either low density lipoproteins (200 μg/ml) or 25hydroxycholesterol (5 μg/ml) as esterificatlon stimuli. Cells treated with these compounds at doses of from 1 to 30 μM showed no impairment of protein synthesis, triglyceride or phospholipld formation, or ability to metabolize 1251-iow density lipoproteins. An Inhibition of cholesterol esterification was seen in human aortic medial cells. With increasing doses of these compounds, low density lipoproteins (25 μg/ml) became progressively less effective in suppressing HMG-CoA reductase in cultured human fibroblasts; with 30 μM cannabidlol the enzyme suppression was only 24' of that found in cells incubated with low density lipoproteins in the absence of drugs. Based on these data, we conclude that the cannabinoids “compartmentalize” cholesterol and, thus, make it unavailable for regulating cellular cholesterol metabolism. This may occur as a result of enhanced sterol efflux. (Arteriosclerosis 1:449-454,1981) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

Cannabinoids Impair the Formation of Cholesteryl Ester in Cultured Human Cells

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Copyright
© 1981 by American Heart Association, Inc.
ISSN
0276-5047

Abstract

The ability of cultured human fibroblasts to form cholesteryl esters from 14C-oleate Is impalred by A'-tetrahydrocannabinol, cannabidiol, and cannabinol, a group of natural products isolated from Cannabls satlwa. This inhibition is compound and dose-related; 30 μM cannabidiol reduced esterlficatlon to less than 20' of the control values. The esteriflcation of endogenous and exogenous cholesterol was affected, since lnhlbition was seen with either low density lipoproteins (200 μg/ml) or 25hydroxycholesterol (5 μg/ml) as esterificatlon stimuli. Cells treated with these compounds at doses of from 1 to 30 μM showed no impairment of protein synthesis, triglyceride or phospholipld formation, or ability to metabolize 1251-iow density lipoproteins. An Inhibition of cholesterol esterification was seen in human aortic medial cells. With increasing doses of these compounds, low density lipoproteins (25 μg/ml) became progressively less effective in suppressing HMG-CoA reductase in cultured human fibroblasts; with 30 μM cannabidlol the enzyme suppression was only 24' of that found in cells incubated with low density lipoproteins in the absence of drugs. Based on these data, we conclude that the cannabinoids “compartmentalize” cholesterol and, thus, make it unavailable for regulating cellular cholesterol metabolism. This may occur as a result of enhanced sterol efflux. (Arteriosclerosis 1:449-454,1981)

Journal

ArteriosclerosisWolters Kluwer Health

Published: Nov 1, 1981

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