Oxidative Stress and Antioxidants in Neurological Diseases: Is There Still Hope?

2017 ◽  
Vol 18 (6) ◽  
pp. 705-718 ◽  
Author(s):  
Andreia Neves Carvalho ◽  
Omidreza Firuzi ◽  
Maria Joao Gama ◽  
Jack van Horssen ◽  
Luciano Saso
Keyword(s):  
Oxidative Stress ◽  
Neurological Diseases

scholarly journals Oxidative Stress and the Microbiota-Gut-Brain Axis

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Laura Dumitrescu ◽  
Iulia Popescu-Olaru ◽  
Liviu Cozma ◽  
Delia Tulbă ◽  
Mihail Eugen Hinescu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurological Diseases ◽  
Brain Lesions ◽  
Brain Inflammation ◽  
Oxygen Species ◽  
Mutual Relationship ◽  
Therapeutic Approaches ◽  
Physiological Regulation ◽  
New Therapeutic Approaches ◽  
Important Pathway

The gut-brain axis is increasingly recognized as an important pathway of communication and of physiological regulation, and gut microbiota seems to play a significant role in this mutual relationship. Oxidative stress is one of the most important pathogenic mechanisms for both neurodegenerative diseases, such as Alzheimer’s or Parkinson’s, and acute conditions, such as stroke or traumatic brain injury. A peculiar microbiota type might increase brain inflammation and reactive oxygen species levels and might favor abnormal aggregation of proteins. Reversely, brain lesions of various etiologies result in alteration of gut properties and microbiota. These recent hypotheses could open a door for new therapeutic approaches in various neurological diseases.

scholarly journals The Neuroprotective Effects of Astaxanthin: Therapeutic Targets and Clinical Perspective

Molecules ◽  
2019 ◽  
Vol 24 (14) ◽  
pp. 2640 ◽  
Author(s):  
Fakhri ◽  
Aneva ◽  
Farzaei ◽  
Sobarzo-Sánchez
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Disorders ◽  
Neurological Disorders ◽  
Spinal Cord Injuries ◽  
Neurological Diseases ◽  
Mechanisms Of Action ◽  
Clinical Perspective ◽  
Neuroprotective Effects ◽  
Brain And Spinal Cord ◽  
Neuronal Disorders

As the leading causes of human disability and mortality, neurological diseases affect millions of people worldwide and are on the rise. Although the general roles of several signaling pathways in the pathogenesis of neurodegenerative disorders have so far been identified, the exact pathophysiology of neuronal disorders and their effective treatments have not yet been precisely elucidated. This requires multi-target treatments, which should simultaneously attenuate neuronal inflammation, oxidative stress, and apoptosis. In this regard, astaxanthin (AST) has gained growing interest as a multi-target pharmacological agent against neurological disorders including Parkinson’s disease (PD), Alzheimer’s disease (AD), brain and spinal cord injuries, neuropathic pain (NP), aging, depression, and autism. The present review highlights the neuroprotective effects of AST mainly based on its anti-inflammatory, antioxidative, and anti-apoptotic properties that underlies its pharmacological mechanisms of action to tackle neurodegeneration. The need to develop novel AST delivery systems, including nanoformulations, targeted therapy, and beyond, is also considered.

Systemic Oxidative Stress Associated with the Neurological Diseases of Aging

2009 ◽  
Vol 34 (12) ◽  
pp. 2122-2132 ◽  
Author(s):  
Jorge A. Serra ◽  
Raúl O. Domínguez ◽  
Enrique R. Marschoff ◽  
Eduardo M. Guareschi ◽  
Arturo L. Famulari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurological Diseases ◽  
Systemic Oxidative Stress

scholarly journals Recent Insights into the Biological Functions of Sestrins in Health and Disease

2017 ◽  
Vol 43 (5) ◽  
pp. 1731-1741 ◽  
Author(s):  
Menglong Wang ◽  
Yao Xu ◽  
Jianfang Liu ◽  
Jing Ye ◽  
Wenhui Yuan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transforming Growth Factor ◽  
Kidney Diseases ◽  
Heart Diseases ◽  
Neurological Diseases ◽  
Mammalian Target Of Rapamycin ◽  
Hypoxia Inducible Factor ◽  
Transforming Growth Factor Β ◽  
Protective Effects ◽  
Immunological Diseases

Sestrins (Sesns) have been identified as a family of highly conserved stress-inducible proteins that are strongly up-regulated by various stresses, including DNA damage, oxidative stress, and hypoxia. The Sesns play protective roles in most physiological and pathological conditions mainly through the regulation of oxidative stress, inflammation, autophagy, endoplasmic reticulum stress, and metabolic homeostasis. In this review, we discussed the possible regulators of Sesns expression, such as p53, forkhead box O, nuclear factor erythroid 2 like 2 (Nrf2), NH (2)-terminal kinase (JNK)/c-Jun pathway and hypoxia-inducible factor-1α (Hif-1α), and the downstream pathways regulated by the Sesns including AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling, mitogen-activated protein kinases (MAPKs) signaling, Nrf2 signaling, NADPH oxidase signaling and transforming growth factor β (TGF-β) signaling in heart diseases, lung diseases, gastrointestinal tract diseases, liver and metabolism diseases, neurological diseases, kidney diseases and immunological diseases. This review aims to provide a comprehensive understanding the protective effects of Sesns.

scholarly journals Gongjin-Dan Enhances Neurite Outgrowth of Cortical Neuron by Ameliorating H2O2-Induced Oxidative Damage via Sirtuin1 Signaling Pathway

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4290
Author(s):  
Hyunseong Kim ◽  
Wanjin Jeon ◽  
Jinyoung Hong ◽  
Junseon Lee ◽  
Changhwan Yeo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Cortical Neurons ◽  
Neurological Diseases ◽  
Preventive Effect ◽  
Neuroprotective Effects ◽  
Mature Neuron ◽  
Pre Treatment ◽  
And Oxidative Stress

Gongjin-dan (GJD) is a multiherbal formula produced from 10 medicinal herbs and has been traditonally used as an oriental medicine to treat cardiovascular diseases, alcoholic hepatitis, mild dementia, and anemia. Additionally, increasing evidence suggests that GJD exerts neuroprotective effects by suppressing inflammation and oxidative stress-induced events to prevent neurological diseases. However, the mechanism by which GJD prevents oxidative stress-induced neuronal injury in a mature neuron remains unknown. Here, we examined the preventive effect and mechanism of GJD on primary cortical neurons exposed to hydrogen peroxide (H2O2). In the neuroprotection signaling pathway, Sirtuin1 is involved in neuroprotective action as a therapeutic target for neurological diseases. After pre-treatment with GJD at three concentrations (10, 25, and 50 µg/mL) and stimulation by H2O2 (30 µM) for 24 h, the influence of GJD on Sirtuin1 activation was assessed using immunocytochemistry, real-time PCR, western blotting, and flow cytometry. GJD effectively ameliorated H2O2-induced neuronal death against oxidative damage through Sirtuin1 activation. In addition, GJD-induced Sirtuin1 activation accelerated elongation of new axons and formation of synapses via increased expression of nerve growth factor and brain-derived neurotrophic factor, as well as regeneration-related genes. Thus, GJD shows potential for preventing neurological diseases via Sirtuin1 activation.

scholarly journals Oxidative stress induces cell death partially by decreasing both mRNA and protein levels of nicotinamide phosphoribosyltransferase in differentiated PC12 cells

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11401
Author(s):  
Cuiyan Zhou ◽  
Weihai Ying
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cell Survival ◽  
Pc12 Cells ◽  
Neurological Diseases ◽  
Biological Effects ◽  
Stress Conditions ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Differentiated Pc12 Cells ◽  
And Oxidative Stress

Background. Multiple studies have indicated crucial roles of NAD+ deficiency in several neurological diseases and aging. It is critical to discover the mechanisms underlying the NAD+ deficiency. A decreased level of Nicotinamide phosphoribosyltransferase (Nampt)—an important enzyme in the salvage pathway of NAD+ synthesis—has been found under certain pathological conditions, while the mechanisms underlying the Nampt decrease are unclear. The purpose of this study is to test the hypothesis that oxidative stress can produce decreased Nampt, and to investigate the biological effects of Nampt on NAD+ synthesis and cell survival under both basal and oxidative stress conditions. Methods. We used differentiated PC12 cells as a cellular model to investigate the effects of oxidative stress on the levels of Nampt. Multiple assays, including flow cytometry-based cell death assays and NAD+ assays were conducted. Results. First, oxidative stress can decrease the levels of Nampt mRNA and Nampt protein; second, Nampt plays significant roles in NAD+ synthesis under both basal conditions and oxidative stress conditions; third, Nampt plays critical roles in cell survival under both basal conditions and oxidative stress conditions; and fourth, oxidative stress produced decreased NAD+ levels and cell survival partially by decreasing Nampt. Collectively, our study has indicated that oxidative stress is a pathological factor leading to decreased Nampt, which plays important roles in oxidative stress-produced decreases in NAD+ levels and cell survival. Our findings have indicated major roles of Nampt in maintaining NAD+ levels and cell survival under both basal and oxidative stress conditions.

scholarly journals Impairment between Oxidant and Antioxidant Systems: Short- and Long-term Implications for Athletes’ Health

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1353 ◽  
Author(s):  
Cristina Nocella ◽  
Vittoria Cammisotto ◽  
Fabio Pigozzi ◽  
Paolo Borrione ◽  
Chiara Fossati ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Exercise Training ◽  
Muscle Damage ◽  
Neurological Diseases ◽  
Cellular Damage ◽  
Antioxidant Systems ◽  
Oxidative Balance

The role of oxidative stress, an imbalance between reactive oxygen species production (ROS) and antioxidants, has been described in several patho-physiological conditions, including cardiovascular, neurological diseases and cancer, thus impacting on individuals’ lifelong health. Diet, environmental pollution, and physical activity can play a significant role in the oxidative balance of an organism. Even if physical training has proved to be able to counteract the negative effects caused by free radicals and to provide many health benefits, it is also known that intensive physical activity induces oxidative stress, inflammation, and free radical-mediated muscle damage. Indeed, variations in type, intensity, and duration of exercise training can activate different patterns of oxidant–antioxidant balance leading to different responses in terms of molecular and cellular damage. The aim of the present review is to discuss (1) the role of oxidative status in athletes in relation to exercise training practice, (2) the implications for muscle damage, (3) the long-term effect for neurodegenerative disease manifestations, (4) the role of antioxidant supplementations in preventing oxidative damages.

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