The differentiation of monocytes into macrophages is a fundamental step for the development of atherogenesis and atherosclerosis. Macrophages participate in lipoprotein accumulation giving rise to foam cells filled with lipid droplets. Several studies seem to suggest an atheroprotective effect of phenolic compounds through a modulation of lipid metabolism. The objective of the present study is to evaluate the role of caffeic acid (CA) and chlorogenic acid (CGA) in counteracting lipid accumulation in a model of monocytes (THP-1) differentiated to macrophages. THP-1-derived macrophages were incubated for 24 h with fatty acids (500 μmol/L oleic/palmitic acid, 2:1 ratio) and phenolic acids (CA and CGA, as single compounds or mix) at different concentrations (0.03, 0.3 and 3 μmol L-1). Lipid accumulation was quantified with the fluorescent dye Nile red. The fluorescence (excitation: 544 nm, emission: 590 nm) was measured in a fluorescence spectrophotometer and the fold increase compared to the control (without fatty acids) was calculated. Data were analysed by one way ANOVA. ANOVA revealed a significant increased lipid accumulation following the fatty acids exposure (p<0.0001). The mix of CA+CGA significantly reduced lipid accumulation at all concentrations tested (-27.5%, -32.0%, -23.4%, respectively at 0.03, 0.3 and 3 μmol L-1; p<0.01). Conversely, no effect was observed following the incubation with the single compounds. Although preliminary, the results seem to indicate a potential effect of CA+CGA, but not of the single phenolics, in counteracting lipids accumulation in THP-1-derived macrophages. The effects were observed at physiological relevant concentrations. Ongoing experiments will be useful to confirm the results obtained and to clarify the potentials mechanisms of action involved in the prevention of the atherogenesis process.
Effect of caffeic and chlorogenic acid in the modulation of lipid accumulation in THP-1-derived macrophages / C. Del Bo’, M. Marino, M. Tucci, P. Riso, M. Porrini. ((Intervento presentato al 3. convegno World Congress on Nutrition and Dietetics tenutosi a Prague nel 2019.
Effect of caffeic and chlorogenic acid in the modulation of lipid accumulation in THP-1-derived macrophages
C. Del Bo’
Primo
;M. MarinoSecondo
;M. Tucci;P. RisoPenultimo
;M. PorriniUltimo
2019
Abstract
The differentiation of monocytes into macrophages is a fundamental step for the development of atherogenesis and atherosclerosis. Macrophages participate in lipoprotein accumulation giving rise to foam cells filled with lipid droplets. Several studies seem to suggest an atheroprotective effect of phenolic compounds through a modulation of lipid metabolism. The objective of the present study is to evaluate the role of caffeic acid (CA) and chlorogenic acid (CGA) in counteracting lipid accumulation in a model of monocytes (THP-1) differentiated to macrophages. THP-1-derived macrophages were incubated for 24 h with fatty acids (500 μmol/L oleic/palmitic acid, 2:1 ratio) and phenolic acids (CA and CGA, as single compounds or mix) at different concentrations (0.03, 0.3 and 3 μmol L-1). Lipid accumulation was quantified with the fluorescent dye Nile red. The fluorescence (excitation: 544 nm, emission: 590 nm) was measured in a fluorescence spectrophotometer and the fold increase compared to the control (without fatty acids) was calculated. Data were analysed by one way ANOVA. ANOVA revealed a significant increased lipid accumulation following the fatty acids exposure (p<0.0001). The mix of CA+CGA significantly reduced lipid accumulation at all concentrations tested (-27.5%, -32.0%, -23.4%, respectively at 0.03, 0.3 and 3 μmol L-1; p<0.01). Conversely, no effect was observed following the incubation with the single compounds. Although preliminary, the results seem to indicate a potential effect of CA+CGA, but not of the single phenolics, in counteracting lipids accumulation in THP-1-derived macrophages. The effects were observed at physiological relevant concentrations. Ongoing experiments will be useful to confirm the results obtained and to clarify the potentials mechanisms of action involved in the prevention of the atherogenesis process.File | Dimensione | Formato | |
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