Table 3.

Studies on OLE (Oleuropein) and OLE aglycone effects on cancer and CVDs in the last five years.

Sample	Treatments	Main Results	Ref.
Human umbilical vein endothelial cells (HUVECs) and dermal microvascular endothelial cells (HMVECs-d-Ad)	OLE (0–50 μM for 18 and 24 h)	OLE does not inhibit VEGFR-2 signaling pathway.	[77]
Mice with colon cancer induced by AOM injections (10 mg/kg, 1 d/week for 6 weeks)	Basal diet either enriched or not with OLE (125  mg/kg), (7 or 17 weeks)	OLE-enriched diet prevents the preneoplastic lesions in different colon segments, reducing the severity of crypt dysplasia and DNA damage in peripheral leukocytes.	[105]
Mouse atrial myocytes (HL-1)	OLE-aglycone (60 μM for 24 h)	Data suggest a possible use of OLE-aglycone to treat human transthyretin (TTR)-related pathologies with the aim to relieve or to delay the occurrence of the most severe cardiac symptoms.	[110]
Luminal MCF-7 breast cancer cell	OLE (100 μM or 200 μM for 72 h)	OLE-induced apoptosis, which is associated with Bax gene expression up-regulation and Bcl2 gene expression down-regulation via p53 pathway activation.	[106]
Thyroid tumorTPC-1 and BCPAP cells	OLE and Ac-OLE (10, 50, and 100 mM for 48 h)	Both treatments inhibit cell proliferation, and decrease H2O2-induced ROS levels, and p-Akt and p-ERK levels. Thus, it exerts antioxidant and inhibitory effects on growth-promoting signal pathways.	[107]
Human colon adenocarcinoma (HT-29) cells	OLE (0 μM–800 μM for 24, 48 and 72 h)	OLE inhibits cell growth and induces apoptosis, which is associated with a decrease in HIF-1α protein and an increase p53, but not to changes in IkB-α and MAPK cascade proteins.	[108]
Hepatocellular carcinoma (Huh7) and human hepatoma (HepG2) cells	OLE (0, 20, 40, 60, 80 or 100 μM for 24 h)	OLE induces apoptosis in HepG2 cells in a dose-dependent manner, via caspase activation which is mediated by changes in proapoptotic Bcl-2 family members, (BAX and Bcl-2) levels, down-regulation of PI3K/AKT signaling pathway, and ROS production increases.	[109]