|
| EVOO, VOO, OO, leaf extracts, and MPCs | Activity | References |
|
| Acetoxypinoresinol | Using DPHH test, it exerts antioxidant effects | [156] |
| Caffeic acid | It inhibits 5-LOX and exerts an antioxidant effects in male rat peritoneal leukocyte triggered by calcium ionophore and PMA | [157] |
| It decreases IL-1β in human blood cultures (sex not reported) stimulated with LPS | [158] |
| EVOO | In healthy men, EVOO reduces urinary excretion of urinary 8‐oxo‐deoxyguanosine by 13% | [159] |
| In 30 hamster males, it reduces atherosclerosis | [160] |
| In ApoE deficient mice (14 females and 22 males), the antiatherogenic effect of EVOO is reduced by dietary cholesterol | [161] |
| In ApoE deficient mice (54 females), EVOO from different cultivars reduces atherosclerotic lesions, plaque size, and macrophage recruitment if compared to diets containing palm oil. EVOO also induces a cholesterol-poor, ApoA-IV-enriched lipoparticles with enhanced arylesterase and antioxidant activities | [162] |
| In male STZ-diabetic rats, it raises BW and HDL and decreases glycaemia, TG, Chol, being ineffective in healthy rats | [163] |
| In STZ-diabetic rats (sex not reported), it elevates HDL and reduces Chol, TG, and LDL | [164] |
| In human platelets obtained from 3 male and 2 female healthy subjects, it reduces NOX2 activation and H2O2 production | [165] |
| In vitro, it inhibits ACE, α‐glucosidase, and α‐amylase being more active vs α‐glucosidase; the richest MPC EVOO is also the most active | [166] |
| Seggianese EVOO extract (rich in secoiridoids) is more active in preventing human LDL oxidation than Taggiasca EVOO extract (rich in lignans) (sex not reported) | [103] |
| In vitro, Spanish EVOO inhibits α-glucosidase, α-amylase, and 5-LOX | [167] |
| LDL and HDL obtained from treated healthy 14 women and 10 men are less oxidizable and are more resistant to lipid peroxidation. Both EVOO and EVOO extract enhance the Chol efflux | [168] |
| In male hypertensive rats, EVOO + olive + leaf rich in HTyr, 3,4 dihydroxyphenylglycol, and oleuropein decreases BP, angiotensin II, and endothelin-1 vs low MPC oil. There are no significant differences in plasma Na+, urea, HDL, and LDL | [169] |
| In an acellular model, HTyr rich extracts have a higher antioxidant and antimutagenic activity than Tyr-rich extract. In HELA cells, the Tyr-rich extract is more effective in increasing GSH whereas ROS levels are not changed by tested EVOO extracts. All extracts upregulate Keap1/Nrf2 pathway | [170] |
| In male mice, high-fat EVOO diet improves glycaemia, insulinemia, glucose tolerance, insulin sensitivity, and insulin secretion. It reduces β-cell apoptosis and normalizes islet glucose metabolism vs high fat lard diet | [171] |
| EVOO extract inhibits p50 and p65 NF-kB translocation in both stimulated and unstimulated PMA-challenged human monocytes and monocyte-derived macrophages (sex not reported) | [172] |
| In ECV304 cells (sex not reported), EVOO extract partially prevents the increase of NO/ET-1 levels induced by high glucose/FFA | [173] |
| In male rats, a bolus of EVOO changes the phospholipids of HDL | [174] |
| Serum obtained from 6 healthy males and 6 females treated with EVOO extract rich in oleuropein and ligstroside reduces the VEGF-stimulated increase in NOX, Nox4, and MMP-9 activities, migration, and invasiveness. It also regulates VEGF-induced morphological differentiation capacity of HUVEC (sex not reported) into capillary-like structures. In human microvascular endothelial cell line, it reduces the VEGF-induced angiogenesis | [175] |
| In male rats, subacute administration of both EVOO rich in MPC and native EVOO with low MPCs reduces ADP platelet aggregation, but acutely only MPC-rich extract reduces ADP induced aggregation | [176] |
| In vitro unfiltered EVOO extract with peptide of low molecular weight inhibits ACE angiotensin converting enzymes in vitro, and in hypertensive male rats, it reduces SBP and DBP | [177] |
| In ApoE deficient mice (sex not reported), extracts (EVOO vs EVOO + polyphenols green tea) enhance macrophage Chol efflux but only EVOO + polyphenols green tea reduces lipid peroxidation | [178] |
| In vitro, Galician EVOO with high level of oleuropein and ligstroside derivatives inhibits the α-amylase and α-glucosidase, being more effective in inhibiting α-glucosidase than acarbose | [167] |
| EVOO vs sunflower oil, sunflower oil + oleic acid, MPC-deprived EVOO, sunflower oil enriched with the MPC of EVOO, and sunflower oil + oleic acid + MPC of EVOO | In all male rats fed with a high-Chol diet, GSH and IL-6 do not vary. EVOO, sunflower oil + MPC of EVOO, and sunflower oil + oleic acid + MPC of EVOO decrease the elevation in MDA and TNF-α levels induced by high-Chol diet | [179] |
| OC-rich EVOO with 1 : 2 oleacein/oleocanthal, 2 : 1 (D2i2) rich in Tyr; EVOO 1 : 2 oleacein/oleocanthal (D2i0.5) rich in Tyr | In healthy men (20 and 50 years), 40 ml of enriched EVOO for one week reduces collagen-stimulated platelet aggregation | [180] |
| OO | In ApoE deficient mice (77 males 63 females), all treatments reduce TG being ineffective versus Chol and vs the number of lesions; however, their dimensions are reduced in females by palm and olive II oils | [181] |
| In 40 male new Zeeland rabbits, dietary supplementation with 15% OO reduces the thrombogenic factors and elevates antithrombotic factors | [182] |
| In male rats, OO reduces and prevents the growth of urinary stones | [183] |
| VOO | In 24 male new Zeeland rabbits, it reduces atherosclerosis | [184] |
| In 40 male new Zeeland rabbits, it reduces atherosclerosis | [182] |
| In human PBMC (sex not reported) and HL60 cells (sex not reported), it inhibits H2O2 and PMA induced DNA damage, being HTyr and Tyr, respectively (extract without verbascoside) | [185] |
| Extract of olive cake vs extract of thyme and vs extract of olive cake + thyme extract | In male rats, single oral administration of the three extracts regulates plasma antioxidant status (DPPH and FRAP) in a time and extract dependent way. In red cells, extracts decrease SOD but increase GPx and CAT | [186] |
| HTyr | In vitro experiments, HTyr and many other phenolic compounds added to standard cell culture media (such as DMEM, MEM, or RPMI) produce H2O2 in the one- to three-digit micromolar range | [187, 188] |
| In alloxan-diabetic male rats, it lowers glycaemia, TG, Chol, alkaline phosphatases, AST and ALT, aspartate and lactate transaminases, lipid peroxidation, total and direct bilirubin, creatinine, urea and increases HDL and hepatic and renal SOD, CAT, and GPx | [189] |
| In alloxan-diabetic male rats, it decreases glycaemia, Chol, and oxidative stress | [190] |
| In STZ-diabetic male rats, it reduces plasma lipid peroxidation, nerve conduction velocity, and thermal nociception and attenuates the decline of sciatic nerve Na+K+ ATPase activity | [191] |
| In STZ-diabetic male rats, it lowers oxidative, nitrosative, and inflammatory biomarkers and platelet aggregation | [192] |
| In STZ-diabetic male rats, it reduces retinopathy, lipid peroxidation, nitrosative stress, TBX2, 6-keto-PGF1α, and IL-β1 | [193] |
| In STZ-diabetic male rats, it lowers retinal ganglion cell number, retinal thickness, and cell size | [193] |
| In STZ-diabetic male rats, it reduces brain lipid peroxidation and inflammation, nitrosative stress, cell death, IL-1β, PGE2 | [194] |
| In STZ-induced diabetic and triton WR-1339 induced hyperlipidemic male mice, it reduces plasma glucose, TG, Chol, lipid peroxidation, TNF-α, CRP and elevates, glucose tolerance, antioxidants, and atherosclerotic index | [195] |
| It prevents metabolic syndrome and inhibits the hepatic and muscular SREBP-1c/FAS pathway reducing oxidative stress and mitochondrial abnormalities and improving lipid and glucose metabolism in db/db C57BL/6J male mice | [196] |
| In the brain of diabetic db/db C57BL/6J male mice, it activates AMPK, SIRT1, and PPARγ coactivator-1α and reduces oxidative stress | [197] |
| In LPS-stimulated human monocytic cells (sex not reported), it suppresses NO release and attenuates the transcription and expression of TNF-α, iNOS, and COX2 in a dose-dependent way | [198] |
| In HUVEC (sex not reported), HTyr and its metabolites suppress TNF-α-induced phosphorylation of NF-κB, ROS production, depletion of GSH, adhesion molecules and downregulate genes encoding antioxidant enzymes. They also reduce the adhesion of human monocytes (cell line) to HUVEC. Finally, they reduce carrageenan induced paw edema and TPA-induced ear edema in male mice | [199] |
| The HTyr pretreatment of HUVEC (sex not reported) suppresses inflammatory angiogenesis induced by PMA and ameliorates mitochondrial function | [200] |
| In male mice, it ameliorates the impact on body adiposity induced by the obesogenic diet | [201] |
| In male rats fed fed with high-fat diet, it reduces AST, ALT, Chol, liver inflammation, and nitrosative/oxidative stress. It improves glucose tolerance, insulin sensitivity, and intestinal barrier integrity and functions and increases hepatic PPARα and its downstream-regulated genes | [202] |
| In male mice fed with diet-induced obesity, it improves glucose homeostasis, insulin signaling markers, chronic inflammation, hepatic steatosis, and endoplasmic reticulum stress | [203] |
| In male rats fed with a diet-induced metabolic syndrome, it reduces adiposity and ameliorates impaired glucose, insulin tolerance, and endothelial dysfunction. It also decreases SBP, left ventricular fibrosis, and resultant diastolic stiffness and markers of liver damage. Notably, the diet used for induction of metabolic syndrome alters HTyr metabolism | [204] |
| In endothelial cells obtained from porcine pulmonary arteries (sex not reported), it increases AMPK, CAT activities, forkhead transcription factor, and cytoprotection against TNF-α-induced damage through the suppression of caspase-3 and NF-kB activation. It also promotes wound healing via Nrf2 synthesis and stabilization | [205, 206] |
| In rat aorta VSMC (sex not reported), it exerts a proapoptotic effect through NO production and protein phosphatase 2A activation with subsequent inactivation of AKT | [207] |
| In male rat peritoneal leukocytes triggered by calcium ionophore, it inhibits 5-LOX and exerts antioxidant effects in leukocytes triggered by PMA | [157] |
| In a female mice model for accelerated aging, it induces the expression of SIRT1 | [208] |
| In vitro, it inhibits human platelet (sex not reported) aggregation induced by ADP and collagen being more active than other MPCs and TBX2 production induced by collagen and thrombin | [209] |
| In pooled human liver microsomes (sex not reported), it inhibits androstenedione 6β-hydroxylase and reductive 17β-HSD activity, whereas it is inactive vs oxidative 17β-HSD | [210] |
| In white adipose of male mice fed with high-fat diet, it reduces the increase in oxidative stress, lipid, and protein oxidation and increases the antioxidant defenses | [211] |
| In adult male rats, it reduces myocardial infarction area, necrosis and apoptosis, the release of LDL and CPK, probably through upregulation of PI3K/AKT pathway | [212] |
| It is a scavenger of hydroxyl radicals, with peroxynitrite and O2− being inactive vs HOCl and H2O2. It protects LDL against oxidation but is not effective vs the oxidation of LDL isolated from humans after HTyr intake (sex not reported) | [213] |
| It inhibits α-glucosidase and α- amylase, being more effective vs α-glucosidase | [214] |
| In human aortic endothelial cells (sex not reported) stimulated with TNF‐α, it significantly reduces the secretion of P‐selectin, ICAM‐1, VCAM‐1, and MCP‐1 | [215] |
| In human HUVEC (sex not reported), it reduces the stimulated tube-like differentiation and the stimulated locomotion, MMP-9 secretion induced by PMA, PMA-stimulated COX2 activity and expression. Pretreatment with HTyr before PMA decreases intracellular ROS and nuclear translocation of the p65 NF-κB subunit and NF-κB transactivation | [216] |
| In male rats, HTyr, 3,4-DHPEA-EA and 3,4-DHPEA-EDA reduce the increase in intracytoplasmic Ca2+ induced by vasopressin. Further, higher concentration of HTyr exerts an endothelium-independent effect. 3,4-DHPEA-EA and 3,4-DHPEA-EDA exert an endothelium-dependent vasodilation in aorta increasing the production of NO | [217] |
| It regulates expression of numerous miRNA in the mice gut (sex not reported) being less effective in other tissues. HTyr administration increases TG | [218] |
| In male mice, it lowers Chol | [219] |
| In human monocytes (sex not reported) stimulated with PMA, it reduces the expression of mRNA and protein of COX2 decreasing PGE2 and O2-production and increases TNF-α production. In human neutrophils (sex not reported) stimulated with PMA, or chemotactic peptide FMLP or opsonized zymosan particles, it does not influence the production of O2− and NOX activity whereas it inhibits the production of H2O2 | [220] |
| In human PBMC (sex not reported) and in human monocytic cell line U937 stimulated with PMA, it reduces the secretion of MMP-9, PGE2 production, COX2 protein expression, and COX2 mRNA without modifying COX1. It inhibits both PGE2 and MMP-9 release from human monocyte-derived macrophages. It suppresses NF-κB activation in human monocytoid cells and reduces PKCα and PKCβ1 activation. Notably, it does not affect MMP-9 and COX2 in basal conditions | [221] |
| In LPS-stimulated human monocytic THP-1 cells (sex not reported), it reduces LPS-stimulated NO and ROS formation in a concentration-dependent way, increases GSH levels, and suppresses the of NF-kB activation | [222] |
| In young male C57BL/6 mice treated with MPC does not modify BW, food intake, and TG but it lowers plasma Chol, leptin. In murine 3T3-L1 preadipocytes, it positively modulates the glutathione-driven antioxidant enzymatic machinery reducing GSSG/GSH ratio, through the modulation of genes related to oxidative stress | [223] |
| In male rats with diet-induced metabolic syndrome, it decreases glucose tolerance, lipids, ALT, AST activity, insulin, weight gain, fat mass, liver steatosis, and ventricular fibrosis | [204] |
| It prevents COX2, TNF-α, DNA damage, and oxidative stress in Balb/c mice treated with LPS (sex not reported) | [224] |
| It increases the TNF-α mRNA level in LPS-activated human monocytes (sex not reported) | [225] |
| HTyr, oleuropein, EVOO extract, homovanillyl alcohol | In HUVEC (sex not reported), EVOO extracts decrease cell surface expression and mRNA of ICAM-1 and VCAM-1. Olea and HTyr are the main actors for these effects. Homovanillyl alcohol inhibits cell surface expression of adhesion molecules, but the effects on mRNA are small | [226] |
HTyr
HTyr- acetate (HTyr-Ac)
HTyr ethyl hydroxytyrosol ether (HTyr-Et) | In male rats fed with high-fat diet, the compounds improve glucose, insulin, leptin levels, lipid peroxidation, and antioxidant capacity status, with HTyr-Ac being the most active. They also reduce the release of inflammatory biomarkers. HTyr-Ac and HTyr-Et improve adipose tissue distribution and adipokine production, decreasing MCP-1 and IL-1β levels | [227] |
| HTyr and homovanillic alcohol | In PBMC obtained by healthy men and women, they inhibit the increase of IL‐1β, MIF, and RANTES induced by oxysterols | [228] |
| HTyr-acetate (HTyr-Ac) | In TNF-α- stimulated HUVEC (sex not reported), it reduces the inflammatory response partly through the TNFRSF1A/SIRT6/PKM2-mediated signaling pathway | [229] |
| HTyr and oleuropein | Both compounds inhibit oxidative burst in human granulocytes and monocytes obtained from healthy individuals (sex not reported) stimulated with PMA. HTyr attenuates the generations of NO and PGE2. In LPS triggered RAW264.7, it reduces NRf2 nuclear translocation and miR-146a expression | [230] |
| HTyr and HTyr-NO | In vascular ring obtained from male rats, it releases NO while HTyr is ineffective. HTyr NO decreases Chol, TG, lipid peroxidation and increases SOD and NO in the serum of STZ-diabetic male mice. Both HTyr-NO and HTyr upregulate SIRT1 expression in the thoracic aorta of male diabetic mice. In HUVEC triggered by hyperglycaemia (sex not reported), HTyr-NO increases cell viability and reduces oxidative stress trough SIRT1 | [231] |
| HTyr, dialdehydic form of elenolic acid linked to HTyr, oleuropein aglycon, oleuropein, Tyr, the dialdehydic form of elenolic acid linked to Tyr, caffeic acid, and verbascoside | In human PBMC and HL60 cells (sex not reported), they inhibit H2O2‐induced DNA damage | [185] |
| HTyr + nicotinate | It inhibits α-glucosidase, and in healthy male mice fed with high-fat diet, it has hypoglycemic, antioxidant, and hypolipidemic activities | [232] |
| HTyr + eicosapentaenoic acid (EPA) | In male mice fed a with high-fat diet, it reduces the steatosis and elevates the hepatic levels of eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), resolvins and attenuates proinflammatory markers | [233] |
| Leaf extract | In INS-1 cells (sex not reported), leaf ethanolic extract and oleuropein improve the damage induced by H2O2. The leaf extract is more potent than oleuropein in preventing the cytotoxic effects and only leaf extract preserves GPx | [234] |
| In STZ-diabetic male rats, the extract ameliorates diabetic alterations | [235] |
| In STZ-diabetic male rats, it decreases glycaemia and HbA1c and increases insulin. It also inhibits α-amylase and α-glucosidase | [236] |
| In acellular model, it inhibits DPPH radical generation. In STZ-diabetic male rats, the extract increases CAT activity, GSH and lowers lipid peroxidation, Chol, TG, histological pancreas, and hepatic damage | [237] |
| In male alloxan-diabetic rats, it shows a hypoglycemic effect and reduces the damage of islets of langerhans | [238] |
| In cultured neonatal rat cardiomyocytes of both sexes, it decreases maximum I (Ca,L) in a reversible manner | [239] |
| Male rats fed with a high-fat diet develop signs of metabolic syndrome. Comparing rats with high-fat diet vs those with high-fat + leaf extract enriched with MPCs, it emerges that leaf extract improves the signs of metabolic syndrome and decreases MDA and uric acid while it is not effective on BP | [240] |
| In human coronary artery endothelial cells (sex not reported) stimulated with serum amyloid A, it reduces the release of IL-6, IL-8, mRNA expression of E-selectin, the phosphorylation of p65 of NF-κB, DNA damage and stabilizes microRNA-146a and let-7e | [241] |
| In male rats, leaf extract containing 20% of HTyr decreases the paw edema induced by carrageenan and IL‐1β and TNF‐α release. It does not affect the anti-inflammatory cytokine IL‐10 | [242] |
| In diet-induced hypercholesterolemic male rats, olive leaf extracts enriched with oleuropein enzymatic and acid hydrolysates rich in oleuropein aglycone and HTyr decrease Chol, TG, and LDL and elevate HDL and serum antioxidant potential. In livers, hearts, kidneys, and aorta lipid peroxidation decreases while liver CAT and SOD increase | [243] |
| Luteolin | It is antioxidant in chemical test and prolongs the lag phase of LDL oxidation. It protects the cells against H2O2 induced damage but it is ineffective vs platelet aggregation (sex not reported) | [209] |
| Oleacein | In vitro, it inhibits angiotensin converting enzyme | [244] |
| It stabilizes atherosclerotic plaque in samples obtained from 20 hypertensive individuals of both sexes | [245] |
| Oleocanthal | It is a nonselective inhibitor of COX1 and 2 and attenuates iNOS and human recombinant 5-LOX, being ineffective vs 15-LOX. Regarding 5-LOX, it is less active than oleuropein and oleacein. In addition, it inhibits TNF-α, IL-1β, IL-6, and GM-CSF | [117, 246, 247] |
| In rat and mouse trigeminal ganglia (females and males used in equal ratio), it acts as agonist of TRPA1 | [248, 249] |
| In male adult rats, it decreases the traumatic injury reducing the inflammatory response by reducing the eNOS and iNOS | [250] |
| In murine chondrogenic ATDC-5 cells and in mouse macrophage J774A.1, it inhibits the LPS-mediated upregulation of NOS2 and LPS induced release of cytokines (sex not reported) | [251] |
| In human monocytes (sex not reported), it reduces the release of O2−, PGE2 and the expression of COX2 and inhibits NAPH-oxidase | [220] |
| Oleuropein | In vitro, it inhibits α-glucosidase and α- amylase | [214] |
| In C2C12 cells (sex not reported), it protects against H2O2 induced damage; further it increases glucose consumption and the phosphorylation of AMPK/ACC and MAPK, but not PI3 kinase/Akt. It improves the insulin sensitivity via insulin-dependent (PI3 kinase/Akt) and insulin independent (AMPK/ACC) | [252] |
| In bovine VSMC (sex not reported), it inhibits cell proliferation in the G1-S phase probably by inhibition of ERK1/2 | [253] |
| In caco cells (sex not reported), it inhibits maltase, human sucrose, glucose transport across Caco-2 monolayers, and uptake of glucose by GLUT2 in Xenopus oocytes; it is a weak inhibitor of human α-amylase | [254] |
| In vitro, it inhibits platelet aggregation being less active than HTyr. In whole blood, collagen platelet aggregation is not modified (sex not reported) | [209] |
| It is antioxidant both in chemical assay and in the lag phase prolonging of LDL oxidation. However it is less active than homovanillic alcohol | [255] |
| In samples of pooled human liver microsomes (sex not reported), it inhibits CYP3A | [256] |
| J774A.1 cells (sex not reported) and in peritoneal macrophages from male mice, it increases the production of NO that is blocked by NOS inhibitor | [257] |
| In male rat peritoneal leukocytes triggered by calcium ionophore, it inhibits 5-LOX and exerts antioxidant effects when leukocytes are stimulated by PMA | [157] |
| In human HUVEC (sex not reported), oleuropein and HTyr reduces the stimulated tube-like differentiation and stimulates locomotion, the increase in MMP-9 secretion induced by PMA without affecting tissue inhibitors of MMP, with this activity being mediated by pretranslation process. It inhibits PMA-stimulated COX2 activity and expression. HTyr before decreases intracellular ROS and nuclear translocation of the p65 NF-κB and its transactivation | [216] |
| In pooled human liver microsomes (sex not reported), they inhibit androstenedione 6β-hydroxylase and 17β-HSD | [210] |
| Oleuropein glycoside | In diluted human blood cultures (sex not reported) stimulated with LPS, it decreases IL-1β | [158] |
| Oleuropein, caffeic acid, Tyr HTyr | In acellular models, they scavenger reactive nitrogen species, with Tyr being the less active; however they do not inhibit the nitrergic transmission in the nerve-stimulated anococcygeus preparation of male rats | [258] |
| Oleuropein-containing supplement OPIACE | In DM2 model (Tsumura Suzuki obese diabetes male) mice, the diet attenuates hyperglycaemia and impairs glucose tolerance and oxidative stress but has no effect on obesity | [259] |
| Olive water methanol extract | In normotensive anaesthetized and atropinized rats (sex not reported), the intravenous administration of extract reduces the BP. In isolated atria of Guinea pig of both sexes, it reduces the spontaneous beating. In isolated thoracic artery of male and female rabbits it reduces K+ and/or phenylephrine induced contraction | [260] |
| Pinoresinol | Using DPHH test, it exerts antioxidant effects being more active than acetoxypinoresinol | [156] |
|
| | In PMA-stimulated RAW 264.7 macrophages (sex not reported), Tyr decreases the O2− and H2O2 generation induced by PMA and scavenges the O2−. These effects seem to be linked with the impairment of (3H)AA release, COX2 expression, PGE2/B4 synthesis, and NO release | [261] |
| | In RAW 264.7 macrophages (sex not reported), triggered by oxLDL-stimulated Tyr reverts H2O2 generation and the AA release and PGE2 production | [262] |
| | In human monocytes (sex not reported) stimulated with PMA, it reduces the production of O2− and the expression of mRNA and protein of COX2, dose-dependently decreasing PGE2 production | [220] |
| Tyr | In RAW 264.7 macrophages (sex not reported), it reduces the activation of iNOS and COX2 gene expression, NF-κB, interferon regulatory factor-1 (IRF-1), and activator of transcription-1α (STAT-1α) induced by gliadin + IFN-γ | [263] |
| | In male rat peritoneal leukocytes triggered by calcium ionophore, it inhibits 5-LOX and exerts antioxidant effects when leukocytes are stimulated by PMA | [157] |
| | In human PBMC (sex not reported) and HL60 cells, it inhibits H2O2‐induced DNA damage | [185] |
| | In PBMC obtained by healthy men and women, it inhibits the increase of IL‐1β, MIF, and RANTES induced by oxysterols | [228] |
|
| Tyr, Tyr glucuronate (Tyr-GLU), and sulfate (Tyr-SUL) | In TNF-α treated-HUVEC (sex not reported), Tyr and Tyr-SUL prevent ROS generation and GSH decrease and downregulate GPx-1, GCL, and OH-1 genes. Tyr-SUL, Tyr, and Tyr-GLU prevent the phosphorylation of NF-κB signaling proteins. Tyr-GLU and Tyr-SUL prevent the increase of genes and proteins expression and secretion of adhesion molecules. In vivo, Tyr and Tyr-SUL, in a dose-dependent manner, ameliorate plantar and ear edemas in male mice | [264] |
| Tyr, oleuropein, and olive pomace | In anoxic EA.hy926 human endothelial cell line (sex not reported), both Tyr and oleuropein attenuate anoxia-induced expression of MMP-9 and MMP-2. Tyr is more efficient than oleuropein in reducing TNF-α. The olive pomace ameliorates all the above parameters and induces time-dependent phosphorylation of p38 MAPK and ERK1/2, and inhibits anoxia-induced NF-κB activation. | [265] |
| Verbascoside | In PBMC (sex not reported) and HL60 cells, it inhibits H2O2− induced DNA damage. | [185] |
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