Antioxidants in suppressing the OS and neuro-gliopathies
Antioxidants | Case | Action | Functional role | References |
---|---|---|---|---|
Carotenoids | Neurodegenerative diseases for instance Huntington’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, epilepsy, schizophrenia, multiple sclerosis, neuropathic pain, and Alzheimer’s disease | Suppresses the oxidative damages | Anti-inflammatory, antioxidants | [59] |
Curcumin | Alzheimer’s disease therapy | Amyloid β peptide (Aβ) treated human neuroblastoma IMR-32 cells | Amyloid-disaggregating properties, antioxidant, anti-inflammatory | [60] |
Dementia therapy | Increased the Aβ-degrading enzymes | Neuroprotective, 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) processing | It modulates membrane fluidity and reduces the OS | The 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 dementia | Stabilizes 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] |
Thioflavones | Neuroprotective agents | Reduces OS | It 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 diseases | Suppresses 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 apoptosis | Reduces inflammatory parameters and OS | Supplementation 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 diseases | Cell death in SH-SY5Y cells via AKT pathway | RA 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 C | Neurodegenerative diseases | Maintain the cellular integrity and apoptosis in mitochondria | Antioxidants and neuroprotective activities in neuropathic pain | [59] |
Vitamin E | Neurodegenerative diseases in neuropathic pain | Maintain the cellular integrity and apoptosis in mitochondria | Antioxidant properties in Alzheimer’s diseases | [59, 66] |
Resveratrol/Y27632/NAD+/ZVAD-FMK | Synapto-protective role | Kinase/Caspase | Y27632 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