Anti-inflammatory and antioxidant effect of lutein

Sl.No.DiseaseMechanism of actionReference
1Neurodegenerative diseaseIn BV-microglia:
Inhibit the synthesis of ROS
↑IL-10
↓TNF-α		[26]
In LPS activated microglia:
Block NF-κB signaling pathway
Regulate the expression of IL-1β, COX-2, iNOS, and TNF-α
Stimulate ERK, finally causes the expression of antioxidant enzymes (NQO1 and HO-1)		[27, 28]
In serious brain injury rats:
↓IL-1β, IL-6, MCP-1, and ROS levels in serum		[32]
In STBI rats:
Inhibit NF-κB protein production		[33]
2Cardiovascular diseaseIn PBMCs:
Blocks NF-κB signaling
Prevents leukocyte adherence and production of inflammatory genes, such as IL-1β, TNF, and IL-6		[35]
Prevent atherosclerosis in mice and guinea pigs by ↓oxidized LDL concentrations, MDA, and cytokine production in aortic tissue[36, 37]
HUVECs:
↓Nitrotyrosine (an ONOO–) index and ROS
↑NO, suppresses the production of adhesion molecules dependent on NF-κB and the interaction between monocytes		[41]
Prevents MI by modulating the MIAT/miR-200a/Nrf2 pathway[46]
3Liver diseaseProtects alcohol-induced liver damage by modulating the NF-κB, Nrf2/HO-1 signaling pathway, ↓SOD and GPx[48, 49]
In ethanol treated rats:
↓NF-κB, COX-2, iNOS, TNF-α, MCP-1, IL-1β, IL-6, AST, ALT, LDH, and sulfhydryl content
↑Nrf2 levels and activities of antioxidant enzymes (catalase, GPx, GSH)		[50]
In guinea pigs fed high cholesterol diet:
PPARα/RXRα-mediated regulation or direct suppression of NF-κB activation (↓levels of mRNA and TNF-α, IL-1β, COX-2, and iNOS)		[51]
Liver ischemia-reperfusion injury in rats:
↓MDA, TNF-α, NF-κB, and IL-1β
Enhance ROS formation and proinflammatory cytokines		[53]
CP toxicities in the liver:
Block NF-κB/p38-MAPK activation and prevent cytokine secretion		[54]
In slow-growing egg-type chicks in ovo:
Regulates PPARγ/RXR pathway and I-κB/NF-κB pathway		[55]
4Eye diseaseIn retinal neural cells:
↓ROS, rhodopsin level, and upregulate GFAP expression		[57]
Inhibit the direct pathway of STAT3 phosphorylation and activation by ROS[58]
In retina treated lutein-PLGA NCs (+PL):
Inhibit NF-κB p65 activity and down-regulate the expression of COX-2 and iNOS		[60]
During optic nerve injury in rats:
↓MDA, IL-1β, and TNF-α, ↑total TSH level in serum		[61]
Anti-cataract effect:
↓Expression of NOS2 and COX-2 through NF-κB		[62]
5Bone diseaseInhibits the expression of RANKL through NF-κB in osteoblasts, which suppresses osteoclast differentiation[42]
Protection against osteoarthritis:
Control oxidative stress and apoptosis through Nrf2 and NF-κB expression		[63]
In LPS-stimulated DC-reduced inflammation and modifying immune response:
↓CD40, co-stimulatory molecule CD86, MHC class II molecule, and IL-6 and ↑production of IL-12 p40		[65]
6DiabetesIn diabetic rats:
↓TNF-α and IL-1β
Inhibit inflammatory response by shielding the proteasome from oxidative stress induced inactivation		[59, 69]
In the retina of Ins2Akita/+ mice:
Inhibit the release of TNF-α and IL-1β and ROS formation		[27, 71]
In diabetic rats:
↓CCT levels of TBARS, caspase-3 TNF-α, IL-1β, and IL-6
Downregulates BDNF, NGF, and IGF. So, oxidative and inflammatory damage as well as neuronal degeneration are also reduced in diabetes		[72]
7Obesity and inflammatory bowel diseaseIn epididymal adipose tissue, downregulate the expression of FAS, PPARγ, and CEBP-α[74]
Lutein nanoparticles, control colitis in mice:
Inhibit NF-κB signaling, TNF-α, iNOS, NLRP3, and IL-1β
↑Expression of ZO-1, claudin-1, and occluding		[76]
8Skin inflammationInhibit the redox-sensitive AP-1 pathway[77, 78]

↑: increasing; ↓: decreasing. ROS: reactive oxygen species; IL-10: interleukin-10; TNF-α: tumor necrosis factor-α; LPS: lipopolysaccharide; NF-κB: nuclear factor kappa B; COX-2: cyclooxygenase-2; iNOS: inducible nitric oxide synthase; HO-1: heme oxygenase-1; STBI: severe traumatic brain injury; PBMCs: peripheral blood mononuclear cells; MI: myocardial infarction; MIAT: MI associated transcript; miR: micro-RNA; Nrf2: nuclear factor erythroid 2-related factor 2; SOD: superoxide dismutase; PPARα: peroxisome proliferator-activated receptor alpha; RXRα: retinoid X receptor alpha; MDA: malondialdehyde; CP: cyclophosphamide; STAT3: signal transducer and activator of transcription 3; RANKL: receptor activator of NF-κB ligand; DC: dendritic cell; TBARS: thiobarbituric acid reactive substances; BDNF: brain-derived neurotrophic factor; NGF: nerve growth factor; IGF: insulin-like growth factor; NLRP3: NOD-like receptor protein 3; ZO-1: zonula occluden-1; GPx: glutathione peroxidase; GSH: glutathione; ERK: extracellular signal-regulated kinase; NQO1: NAD(P)H quinone oxidoreductase 1; MCP-1: monocyte chemoattractant protein-1; LDL: low-density lipoprotein; AP-1: activator protein-1; HUVECs: human umbilical vein endothelial cells; AST: aspartate transaminase; ALT: alanine transaminase; LDH: lactate dehydrogenase; I-κB: inhibitor of kappa B; GFAP: glial fibrillary acidic protein; PLGA: poly(lactic-co-glycolic acid); NCs: neural crest cells; PL: phospholipid; TSH: thyroid stimulating hormone; MHC: major histocompatibility complex; Ins2: insulin 2; FAS: Fas cell surface death receptor; CEBP-α: CCAAT/enhancer-binding protein alpha; CCT: cerebral cortex