ArticleScientific reports2025
D-limonene modulates AMPK signaling to inhibit ox-LDL-induced foam cell formation.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
One of the primary mechanisms of atherosclerosis involves foam cell formation induced by oxidized low-density lipoprotein (ox-LDL). This study aims to explore the potential of D-limonene to inhibit ox-LDL-induced foam cell formation by activating the AMPK signaling pathway. THP-1 cells were differentiated into macrophages using PMA and subsequently divided into five groups: Control, ox-LDL, ox-LDL + LIM 25 µM, ox-LDL + LIM 50 µM, and ox-LDL + LIM 100 µM. Cell viability was assessed using the CCK-8 assay, foam cell formation was evaluated by Oil Red O staining, and inflammatory factor levels (IL-1β, IL-18, TNF-α) were measured using ELISA. Autophagosome formation was detected via immunofluorescence, and protein expressions related to foam cell formation and autophagy were analyzed by Western blotting. ox-LDL treatment markedly increased lipid accumulation, cholesterol levels, and inflammatory cytokine expression in macrophages while reducing autophagosome formation. D-limonene treatment significantly decreased the expression of SR-A and CD36, enhanced ABCA1 and ABCG1 levels, and reduced inflammatory cytokine levels. Additionally, autophagy-related proteins LC3-II/LC3-I, Atg5, and Beclin-1 were restored. D-limonene activated AMPK/p-AMPK and inhibited mTOR/p-mTOR signaling. By modulating the AMPK/mTOR signaling pathway, D-limonene effectively inhibits ox-LDL-induced foam cell formation and inflammation, suggesting a potential protective effect of D-limonene in ox-LDL-induced foam cell formation, which may provide experimental evidence for future in vivo studies on atherosclerosis.
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