TABLE 2.
Study type | Study subjects | Dose | Duration | Major functions | Molecular biomarkers | References |
---|---|---|---|---|---|---|
Animal studies | HgCl2‐induced Wistar rats (40 rats) | 5 mL/kg body weight (oral gavage and injection) | 2 days | Antioxidation |
MDA, ROS↓ GSH‐Px, SOD, GSH↑ |
Yang et al. (2011) |
Male albino rats (24 adult rats) | 10 mg/kg. BW (orally) | 5 weeks | Antioxidation |
MDA, LPO, Total nitrate/nitrite↓ GSH, SOD, TAC↑ |
Mansour and Tawfik (2012) | |
Cisplatin‐induced male Wistar rats (28 rats) | 6 mg/kg. BW/day (Single‐injection) | 10 days | Antioxidation, anti‐inflammation |
NF‐κB p65↓ Nrf2, and HO‐1↑ GSH, CAT, GPx, and SOD↑ |
Sahin et al. (2010) | |
Colistin‐induced female Kunming mice | 5 or 20 mg/kg. BW/day (orally) | 7 days | Antioxidation |
LPO↓ HO‐1↑ Nrf2, HO‐1 mRNA↑ GSH, CAT, SOD↑ NF‐κB mRNA↓ |
Dai et al. (2015) | |
Croton oil‐induced male Kunming mice | 0.5 g/kg (oral gavage) | 4 days | Anti‐inflammation | Edema rate↓ | Yaping et al. (2003) | |
Streptozotocin‐induced diabetic Wistar rats | 1, 2 and 4 mg/kg | 10 weeks | Antioxidation, anti‐inflammation |
Oxidative stress, NO↓ TNF‐α production↓ |
Kuhad, Sethi, and Chopra (2008) | |
Hyperhomocysteinemic Sprague–Dawley rats (50 rats) | 10, 15, and 20 mg/kg | 12 weeks | Anti‐inflammation | VCAM‐1, MCP‐1, IL‐8↓ | Liu et al. (2007) | |
Alcohol‐fed Fischer 344 rats (60 rats) | 1.1, 3.3 mg/kg. BW/day | 11 weeks | Anti‐inflammation | TNF‐α mRNA, hepatic inflammatory foci↑ | Veeramachaneni et al. (2008) | |
Ovalbumin (OVA)‐induced BALB/c mice | 8 or 16 mg/kg BW/day in 200 μL (IP injection) | 3 days | Anti‐inflammation |
IFN‐γ and T‐bet mRNA↑ IL‐4 mRNA↓ |
Lee et al. (2008) | |
Young male and female rats (48 rats/sex) | 0, 267, 534, 1068 mg/kg. BW | 30 days | Antioxidation |
CAT, SOD & GSH‐Px↑ MDA, ROS formation↓ |
Hu et al. (2013) | |
28 male Wistar‐Albino male rats | 10 mg/kg. BW/day | 28 days | Antioxidation |
Blood glucose and HbA1c↓ Oxidative DNA damage↓ 8‐OHdG↓ |
Karahan et al. (2018) | |
Clinical trials | Prostate cancer patients (32 men) | 30 mg/day | 3 weeks | Antioxidation | Oxidative DNA damage↓ | Chen et al. (2001) |
Type 2 diabetic patients (57 patients) | 500 mL/day | 4 weeks | Antioxidation |
Plasma lycopene level (3‐fold)↑ LDL resistance to oxidation↑ |
Upritchard et al. (2000) | |
Healthy, normolipidemic female volunteers (12 females) | 8 mg/day | 3 weeks | Antioxidation |
Plasma lycopene level↑ 8 iso‐PGF2α in urine↓ LDL susceptibility to oxidation↓ |
Visioli et al. (2003) | |
Well‐nourished, healthy elderly persons (33 female and 20 male) | 330 mL/day tomato or, 47.1 mg lycopene | 8 weeks | Immunomodulation |
Plasma lycopene level↑ TNF‐α, and IL‐4↑ IL‐2↓ |
Watzl et al. (2000) | |
Healthy young volunteers (26 individuals) | 5.7 mg | 26 days | Anti‐inflammation | TNF‐α↓ | Riso et al. (2006) | |
Healthy, non‐smoking post‐menopausal women (37 women) | 4 mg/day (mixed supplementation) and 12 mg/day (individually) | 56 days | Antioxidation | Oxidative DNA damage↓ | Zhao et al. (2006) | |
Cell level study | Lipopolysaccharide (LPS)‐mediated (RAW 264.7) Murine macrophages | 0.5, 1, 2 μM | 24 h | Anti‐inflammation |
IL‐6 and IL‐1β mRNA↓ JNK phosphorylation↓ |
Marcotorchino et al. (2012) |
Lipopolysaccharide (LPS)‐mediated (RAW 264.7) macrophages |
1–10 μM |
24 h | Antioxidation, anti‐inflammation |
mRNA of iNOS, NO↓ IL‐6↓ p38, ERK1/2, IκB phosphorylation↓ NF‐κB translocation↓ |
Feng et al. (2010) | |
THP‐1 (human monocytic cell line) |
0.5–2 μM |
6 h | Antioxidation, anti‐inflammation |
IL‐8↓ ROS and NOX‐4↓ NF‐κB DNA binding, NF‐κB/p65 nuclear translocation↓ IKKα and IκBα phosphorylation↓ ERK1/2, JNK, p38 MAPK phosphorylation↓ |
Simone et al. (2011) | |
0.5–2 μM | 24 h | Antioxidation, anti‐inflammation |
ROS and 8‐OHdG formation↓ NOX‐4 and NADPH oxidase↓ Hsp70, Hsp90 expressions↓ p38, ERK, JNK, MAPK phosphorylation↓ |
Palozza et al. (2010) | ||
3 T3‐L1 (murine pre‐adipocytes) | 0.5, 1, or 2 μM | 24 h | Anti‐inflammation | mRNA expression of IL‐6, MCP‐1, IL‐1β, RANTES, CXCL1, CXCL10, SAA3, and haptoglobin↓ | Gouranton et al. (2011) | |
LPS‐induced Human umbilical vein endothelial cells (HUVECs) | 0–20 μM | 6 h | Anti‐inflammation |
HMGB1, HMGB1‐mediated TNF‐α and sPLA2‐IIA↓ VCAM‐1, ICAM‐1, E‐selectin↓ TLR‐2, TLR‐4, and receptors of RAGE↓ |
Lee et al. (2012) |
Note: ↑ = increase; ↓ = decrease/inhibit; → = normal/no change.
Abbreviations: 8‐OHdG, 8‐hydroxy‐2′‐deoxyguanosine; CAT, catalase; CXCL, chemokine (C‐X‐C motif) ligand; ERK, extracellular signal‐regulated kinases; GSH, glutathione; GSH‐Px, glutathione peroxidase; HMGB1, high mobility group box 1; HO‐1, heme oxygenase‐1; ICAM‐1, intercellular adhesion molecule‐1; IFN‐α, interferon type I; IKKα, IκB kinase α; IL, interleukin; iNOS, inducible nitric oxide synthase; JNK, c‐Jun N‐terminal kinases; LPO, lipid peroxidation; MAPK, mitogen‐activated protein kinases; MCP‐1, monocyte chemoattractant protein‐1; MDA, malondialdehyde; NF‐κB, nuclear factor kappa B; NO, nitric oxide; NOX4, NADPH oxidase 4; Nrf2, nuclear factor erythroid 2–related factor 2; PGF2α, prostaglandin F2α; RANTES, regulated upon activation, normal T cell expressed and presumably secreted; SOD, superoxide dismutase; sPLA2‐IIA, group II secretory phospholipase A; TLR, toll‐like receptor; TNF‐α, tumor necrosis factor‐alpha; VCAM‐1, vascular cell adhesion molecule‐1.