Decaffeinated coffee and green tea extract inhibit foam cell atherosclerosis by lowering inflammation and improving cholesterol influx/efflux balance through upregulation of PPARγ and miR-155 [version 2; peer review: awaiting peer review]

Background: Foam cells, the markers of early atherosclerosis and characterise the advanced atherosclerotic plaque, are stimulated by inflammation due to the excess of lipid in macrophages. The combination of decaffeinated coffee and green tea extract (DCGTE) has been suggested to have a role in foam cell inhibition. Objective: to investigate the role of DCGTE against foam cell formation, through modulation of the inflammation process and cholesterol metabolism in macrophage colony stimulating factor (M-CSF) and oxidized low-density lipoprotein (oxLDL)-exposed macrophages. Methods: Coffee and green tea were extracted by filtration and infusion respectively. Both of coffee and green tea underwent decaffeination using active carbon and blanching methods, respectively. Raw 264.7 Cells were administered with 160/160 and 320/320 μg/ml of DCGTE. Foam cell formation was observed using a light microscope after staining with Oil Red O (ORO), and quantified with ELISA. The expression of cluster differentiation 36 (CD36) ( lipid influx) and ATP binding cassette transporter A1 (ABCA1) ( cholesterol efflux) were determined through immunofluorescence. Tumor Necrosis Factor α (TNFα) and Interleukin10 (IL10) were quantified with ELISA. Peroxisome proliferator activated response γ (PPARγ) expression and activity were assessed with Polymerase Chain Reaction (PCR) and ELISA, respectively. The expression of microRNA 155 (miR-155) was examined using qPCR. Results: DCGTE at the above concentrations tended to reduce foam cell numbers, significantly inhibited lipid accumulation (p=0.000), reduced CD36 expression (p=0.000) and TNFα secretion (p=0.000) in Raw264.7 exposed to M-CSF 50 ng/ml and oxLDL 50 μg/ml. The PPARγ expression (p=0.000), PPARγ activity (p=0.001), ABCA1 (p=0.002), miR-155 relative expression (p=0.000), and IL10 production (p=0.000) also increased in DCGTE groups. Conclusion: DCGTE lowered foam cell possibly through attenuation of the inflammatory process and improvement of lipid/efflux mechanisms via upregulation of PPARγ and miR-155 in M-CSF and oxLDL-stimulated Raw264.7 cells. Our results suggest DCGTE might help to prevent atherosclerosis-based diseases.