An in vitro experiment evaluated the results induced by various flavonoids on the arachidonic acid release from rat neutrophils; kaempferol, luteolin, quercetin and amentoflavone reduced the inflammatory response and inhibited the activity of β-glucuronidase and lysozyme (Tordera et al., 1994). Furthermore, the positive outcome of Brassica oleracea extracts (water and methanol respectively) for CVD risk were examined; for this purpose, HUVECs were exposed to the extracts (24 h) and then to TNF-α stimulation. Exposure to the extracts from Brassica oleracea significantly reduced the TNF-α induced expression of E-selectin, ICAM-1 and VCAM-1 (Kuntz and Kunz, 2014). Another study demonstrated the capacity of extracts from Mango (Mangifera indica L.) to counteract TNF-α effects on HUVECs, through the inhibition of IL-6, IL-8, COX-2 and ICAM-1, while restoring the expression of eNOS usually down-regulated by TNF-α (Mura et al., 2015). Interestingly, in an animal model, for example, supplementation of standard chow with cacao phenolic compounds in apolipoprotein E-deficient mice, lead to an anti-inflammatory effect justified by a reduction of VCAM-1 and ICAM-1 expressions, a decrease of oxidative stress markers and a reduction of cholesterol accumulation in plaque compared to control (Natsume and Baba, 2014). Likewise, propolis (green, red or brown) treatment induced a reduction of MCP-1, VCAM, PECAM, FGF, PDGF, VEGF, MMP-9 and upregulated tissue inhibitor of metalloproteinases 1 (TIMP-1) in initial atherosclerotic lesions in LDL receptor gene knockout mice fed a diet rich in cholesterol for inducing atherosclerotic lesions; only red propolis upregulated heme oxygenase 1 (HO-1) and TIMP-1 in advanced atherosclerotic lesions (Daleprane et al., 2012).