Terpene Lactucopicrin Limits Macrophage Foam Cell Formation by a Reduction of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 in Lipid Rafts.

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Tytuł:: Terpene Lactucopicrin Limits Macrophage Foam Cell Formation by a Reduction of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 in Lipid Rafts.
Autorzy:: Li Q; Department of Nutrition, School of Public Health, Sun Yat-sen University (Northern Campus), Guangzhou, P. R. China.
Liu X; Department of Nutrition, School of Public Health, Sun Yat-sen University (Northern Campus), Guangzhou, P. R. China.
Zhang X; Department of Nutrition, School of Public Health, Sun Yat-sen University (Northern Campus), Guangzhou, P. R. China.
Du Y; Department of Nutrition, School of Public Health, Sun Yat-sen University (Northern Campus), Guangzhou, P. R. China.
Chen G; Department of Nutrition, School of Public Health, Sun Yat-sen University (Northern Campus), Guangzhou, P. R. China.
Xiang P; Department of Nutrition, School of Public Health, Sun Yat-sen University (Northern Campus), Guangzhou, P. R. China.
Ling W; Department of Nutrition, School of Public Health, Sun Yat-sen University (Northern Campus), Guangzhou, P. R. China.; Guangdong Provincial Key Laboratory for Food, Nutrition and Health, Guangzhou, P. R. China.; Guangdong Engineering Technology Research Center for Nutrition Translation, Guangzhou, P. R. China.
Wang D; Department of Nutrition, School of Public Health, Sun Yat-sen University (Northern Campus), Guangzhou, P. R. China.; Guangdong Provincial Key Laboratory for Food, Nutrition and Health, Guangzhou, P. R. China.; Guangdong Engineering Technology Research Center for Nutrition Translation, Guangzhou, P. R. China.
Źródło:: Molecular nutrition & food research [Mol Nutr Food Res] 2022 Feb; Vol. 66 (4), pp. e2100905. Date of Electronic Publication: 2021 Dec 29.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Original Publication: Weinheim, Germany : Wiley-VCH, c2004-
MeSH Terms:: Foam Cells*
Scavenger Receptors, Class E*
Animals ; Humans ; Lactones ; Lipoproteins, LDL/metabolism ; Macrophages ; Membrane Microdomains ; Mice ; Sesquiterpenes ; Terpenes/pharmacology
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Contributed Indexing:: Keywords: atherosclerosis; foam cell; lactucopicrin; lectin-like oxidized low-density lipoprotein receptor-1; lipid raft
Substance Nomenclature:: 0 (Lactones)
0 (Lipoproteins, LDL)
0 (Scavenger Receptors, Class E)
0 (Sesquiterpenes)
0 (Terpenes)
6466-74-6 (intybin)
Entry Date(s):: Date Created: 20211221 Date Completed: 20220331 Latest Revision: 20220401
Update Code:: 20240104
DOI:: 10.1002/mnfr.202100905
PMID:: 34932892
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Scope: Sustained inflammation promotes macrophage foam cell formation by promoting cholesterol influx and impairing cholesterol efflux. Terpene lactucopicrin, affluent in vegetables of the Asteraceae family (e.g., chicory, curly escarole, and lettuce) can inhibit atherogenesis in mice. However, it remains unknown whether and how lactucopicrin regulates macrophage foam cell formation.
Methods and Results: Lactucopicrin at physiologically reachable concentrations inhibits oxidized low-density lipoprotein (oxLDL)-induced foam cell formation in inflammatory mouse bone marrow derived macrophages established by 50 pg mL -1 of LPS, reachable level in patients with metabolic endotoxemia. This effect is not due to modulation of cholesterol efflux, but reliant on a reduction in lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1)-mediated cholesterol influx. Mechanistically, lactucopicrin does not affect LOX-1 expression, cellular oxidative stress, and exocytosis, known mechanisms regulating LOX-1 function in cholesterol influx. Strikingly, lactucopicrin selectively decreases LOX-1 content in lipid rafts, an effect responsible for the lactucopicrin effect on cholesterol influx. Moreover, ApoE -/- mice fed a high fat diet supplemented with lactucopicrin for 12 weeks display fewer macrophage foam cells within atherosclerotic plaques relative to the control mice.
Conclusion: Lactucopicrin limits macrophage foam cell formation through a reduction of LOX-1 distribution in lipid rafts, thus contributing to its atheroprotective effect.
(© 2021 Wiley-VCH GmbH.)

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