Antioxidants in suppressing the OS and neuro-gliopathies

AntioxidantsCaseActionFunctional roleReferences
CarotenoidsNeurodegenerative diseases for instance Huntington’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, epilepsy, schizophrenia, multiple sclerosis, neuropathic pain, and Alzheimer’s diseaseSuppresses the oxidative damagesAnti-inflammatory, antioxidants[59]
CurcuminAlzheimer’s disease therapyAmyloid β peptide (Aβ) treated human neuroblastoma IMR-32 cellsAmyloid-disaggregating properties, antioxidant, anti-inflammatory[60]
Dementia therapyIncreased the Aβ-degrading enzymesNeuroprotective, suppresses TNF, formation of Aβ plaque, and also protects the brain cells from noxious agents[61]
Fatty acids (DHA)Enhances non-amyloidogenic amyloid precursor protein (APP) processingIt modulates membrane fluidity and reduces the OSThe increased membrane fluidity and non-amyloidogenic processing of APP enhanced the secretion of sAAPα in Alzheimer’s disease HEK293 cells. This increased secretion of sAAPα protects against apoptosis[62]

Epigallocatechin-3-gallate

Extracted from Camelia sinensis

Reduces the risk of Alzheimer’s disease and age-related dementiaStabilizes the mitochondrial function such as adenosine triphosphate (ATP)

It regulates the p-glycoprotein.

It also shows antiapoptotic and antioxidative activities that directly inhibit Aβ plaque formation

[61]
ThioflavonesNeuroprotective agentsReduces OSIt activates the anti-apoptotic cell survival proteins of PI3K/Akt and ERK1/2 pathway in neuroblastoma cell lines[63]
Ginsenosides (GRg1 and GRg3, extracted from Ginseng)Neuroprotective effect in Alzheimer’s diseasesSuppresses the Aβ associated neurotoxicity as linked with ROS

Ginsenosides regulate acetylcholine receptor channels, as these channels are linked with learning and memory.

GRg1 significantly suppresses the Aβ associated neurotoxicity.

GRg3 significantly reduces the amyloid-β40 and amyloid β42 level in the treatment of the brain of the transgenic mice.

GRg3 also protects against glutamate-induced neurotoxicity

[61]
Quercetin (flavonoids)Oxidative stress and apoptosisReduces inflammatory parameters and OSSupplementation of quercetin decreases the neuronal damage, scavenges the free radicals by PCB, and prevents PCB-induced PCB and OS in rat brains[64]
Retinoic acid (RA)Proteosome inhibition in neurodegenerative diseasesCell death in SH-SY5Y cells via AKT pathwayRA treatment of cultured neuroblastoma cells under which proteasome inhibition results in the accumulation of ubiquitinated protein loses its ability to kill the cells and thus shows the protective role in neurodegenerative diseases[65]
Vitamin CNeurodegenerative diseasesMaintain the cellular integrity and apoptosis in mitochondriaAntioxidants and neuroprotective activities in neuropathic pain[59]
Vitamin ENeurodegenerative diseases in neuropathic painMaintain the cellular integrity and apoptosis in mitochondriaAntioxidant properties in Alzheimer’s diseases[59, 66]
Resveratrol/Y27632/NAD+/ZVAD-FMKSynapto-protective roleKinase/CaspaseY27632 and NAD+ showed a strong synaptoprotective role in the neuronal culture of mice brains, whereas resveratrol and ZVAD-FMK failed to show neuroprotective function[67]

DHA: docosahexaenoic acid; GRg1: ginsenoside Rg1; NAD+: nicotinamide adenine dinucleotide; AKT: protein kinase B; sAAPα: soluble α-amyloid precursor protein; PI3K: phosphoinositide 3-kinases; ERK1/2: extracellular signal-regulated kinase 1/2; PCB: polychlorinated biphenyls