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20 pages, 3508 KiB

Open AccessArticle

Hesperetin Nanocrystals Improve Mitochondrial Function in a Cell Model of Early Alzheimer Disease

by Lukas Babylon, Rekha Grewal, Pascal-L. Stahr, Ralph W. Eckert, Cornelia M. Keck and Gunter P. Eckert

Antioxidants 2021, 10(7), 1003; https://doi.org/10.3390/antiox10071003 - 23 Jun 2021

Cited by 18 | Viewed by 3465

Abstract

Mitochondrial dysfunction represents a hallmark of both brain aging and age-related neurodegenerative disorders including Alzheimer disease (AD). AD-related mitochondrial dysfunction is characterized by an impaired electron transport chain (ETC), subsequent decreased adenosine triphoshpate (ATP) levels, and elevated generation of reactive oxygen species (ROS). [...] Read more.

Mitochondrial dysfunction represents a hallmark of both brain aging and age-related neurodegenerative disorders including Alzheimer disease (AD). AD-related mitochondrial dysfunction is characterized by an impaired electron transport chain (ETC), subsequent decreased adenosine triphoshpate (ATP) levels, and elevated generation of reactive oxygen species (ROS). The bioactive citrus flavanone hesperetin (Hst) is known to modulate inflammatory response, to function as an antioxidant, and to provide neuroprotective properties. The efficacy in improving mitochondrial dysfunction of Hst nanocrystals (HstN) with increased bioavailability has not yet been investigated. Human SH-SY5Y cells harboring neuronal amyloid precursor protein (APP₆₉₅) acted as a model for the initial phase of AD. MOCK-transfected cells served as controls. The energetic metabolite ATP was determined using a luciferase-catalyzed bioluminescence assay. The activity of mitochondrial respiration chain complexes was assessed by high-resolution respirometry using a Clarke electrode. Expression levels of mitochondrial respiratory chain complex genes were determined using quantitative real-time polymerase chain reaction (qRT-PCR). The levels of amyloid β-protein (Aβ_1-40) were measured using homogeneous time-resolved fluorescence (HTRF). ROS levels, peroxidase activity, and cytochrome c activity were determined using a fluorescence assay. Compared to pure Hst dissolved in ethanol (HstP), SH-SY5Y-APP₆₉₅ cells incubated with HstN resulted in significantly reduced mitochondrial dysfunction: ATP levels and respiratory chain complex activity significantly increased. Gene expression levels of RCC I, IV, and V were significantly upregulated. In comparison, the effects of HstN on SY5Y-MOCK control cells were relatively small. Pure Hst dissolved in ethanol (HstP) had almost no effect on both cell lines. Neither HstN nor HstP led to significant changes in Aβ_1-40 levels. HstN and HstP were both shown to lower peroxidase activity significantly. Furthermore, HstN significantly reduced cytochrome c activity, whereas HstP had a significant effect on reducing ROS in SH-SY5Y-APP₆₉₅ cells. Thus, it seems that the mechanisms involved may not be linked to altered Aβ production. Nanoflavonoids such as HstN have the potential to prevent mitochondria against dysfunction. Compared to its pure form, HstN showed a greater effect in combatting mitochondrial dysfunction. Further studies should evaluate whether HstN protects against age-related mitochondrial dysfunction and thus may contribute to late-onset AD. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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21 pages, 2161 KiB

Open AccessArticle

Moringa oleifera Protects SH-SY5YCells from DEHP-Induced Endoplasmic Reticulum Stress and Apoptosis

by Ines Amara, Maria Laura Ontario, Maria Scuto, Gianluigi Maria Lo Dico, Sebastiano Sciuto, Valentina Greco, Salwa Abid-Essefi, Anna Signorile, Angela Trovato Salinaro and Vittorio Calabrese

Antioxidants 2021, 10(4), 532; https://doi.org/10.3390/antiox10040532 - 29 Mar 2021

Cited by 24 | Viewed by 3367

Abstract

Moringa oleifera (MO) is a medicinal plant that has been shown to possess antioxidant, anticarcinogenic and antibiotic activities. In a rat model, MO extract (MOe) has been shown to have a protective effect against brain damage and memory decline. As an extending study, [...] Read more.

Moringa oleifera (MO) is a medicinal plant that has been shown to possess antioxidant, anticarcinogenic and antibiotic activities. In a rat model, MO extract (MOe) has been shown to have a protective effect against brain damage and memory decline. As an extending study, here, we have examined the protective effect of MOe against oxidative stress and apoptosis caused in human neuroblastome (SH-SY5Y) cells by di-(2-ethylhexyl) phthalate (DEHP), a plasticizer known to induce neurotoxicity. Our data show that MOe prevents oxidative damage by lowering reactive oxygen species (ROS) formation, restoring mitochondrial respiratory chain complex activities, and, in addition, by modulating the expression of vitagenes, i.e., antioxidant proteins Nrf2 and HO-1. Moreover, MOe prevented neuronal damage by partly inhibiting endoplasmic reticulum (ER) stress response, as indicated by decreased expression of CCAAT-enhancer-binding protein homologous protein (CHOP) and Glucose-regulated protein 78 (GRP78) proteins. MOe also protected SH-SY5Y cells from DEHP-induced apoptosis, preserving mitochondrial membrane permeability and caspase-3 activation. Our findings provide insight into understanding of molecular mechanisms involved in neuroprotective effects by MOe against DEHP damage. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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16 pages, 2396 KiB

Open AccessArticle

Effect-Directed Profiling of Powdered Tea Extracts for Catechins, Theaflavins, Flavonols and Caffeine

by Gertrud E. Morlock, Julia Heil, Antonio M. Inarejos-Garcia and Jens Maeder

Antioxidants 2021, 10(1), 117; https://doi.org/10.3390/antiox10010117 - 15 Jan 2021

Cited by 29 | Viewed by 3835

Abstract

The antioxidative activity of Camelia sinensis tea and especially powdered tea extracts on the market, among others used as added value in functional foods, can considerably vary due to not only natural variance, but also adulteration and falsification. Thus, an effect-directed profiling was [...] Read more.

The antioxidative activity of Camelia sinensis tea and especially powdered tea extracts on the market, among others used as added value in functional foods, can considerably vary due to not only natural variance, but also adulteration and falsification. Thus, an effect-directed profiling was developed to prove the functional effects or health-promoting claims. It took 3–12 min per sample, depending on the assay incubation time, for 21 separations in parallel. Used as a fast product quality control, it can detect known and unknown bioactive compounds. Twenty tea extracts and a reference mixture of 11-bioactive compounds were investigated in parallel under the same chromatographic conditions by a newly developed reversed phase high-performance thin-layer chromatographic method. In eight planar on-surface assays, effect-directed tea profiles were revealed. Catechins and theaflavins turned out to be not only highly active, but also multi-potent compounds, able to act in a broad range of metabolic pathways. The flavan-3-ols acted as radical scavengers (DPPH^∙ assay), antibacterials against Gram-positive Bacillus subtilis bacteria, and inhibitors of tyrosinase, α-glucosidase, β-glucosidase, and acetylcholinesterase. Further effects against Gram-negative Aliivibrio fischeri bacteria and β-glucuronidase were assigned to other components in the powdered tea extracts. According to their specifications, the activity responses of the powdered tea extracts were higher than in mere leaf extracts of green, white and black tea. The multi-imaging and effect-directed profiling was not only able to identify known functional food ingredients, but also to detect unknown bioactive compounds (including bioactive contaminants, residues or adulterations). Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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10 pages, 263 KiB

Open AccessArticle

Association of Antioxidants Use with All-Cause and Cause-Specific Mortality: A Prospective Study of the UK Biobank

by Inken Behrendt, Gerrit Eichner and Mathias Fasshauer

Antioxidants 2020, 9(12), 1287; https://doi.org/10.3390/antiox9121287 - 16 Dec 2020

Cited by 8 | Viewed by 2775

Abstract

Prospective studies and randomized controlled trials elucidating the impact of antioxidants supplementation on mortality risk are inconclusive. The present analysis determined association between regular antioxidants use and all-cause (primary objective), as well as cause-specific, mortality in 345,626 participants of the UK Biobank cohort [...] Read more.

Prospective studies and randomized controlled trials elucidating the impact of antioxidants supplementation on mortality risk are inconclusive. The present analysis determined association between regular antioxidants use and all-cause (primary objective), as well as cause-specific, mortality in 345,626 participants of the UK Biobank cohort using Cox proportional hazard models. All models were adjusted for confounders and multiple testing. Antioxidants users were defined as participants who indicated to regularly use at least one of the following: multivitamins, vitamin C, vitamin E, selenium, and zinc. Median age of antioxidants users (n = 101,159) and non-users (n = 244,467) at baseline was 57 years. During 3.9 million person-years and a median follow-up of 11.5 years, 19,491 deaths occurred. Antioxidants use was not significantly associated with all-cause, cancer, and non-cancer mortality including several cancer and non-cancer subtypes. Interestingly, mortality risk from respiratory disease was significantly 21% lower among antioxidants users as compared to non-users (hazard ratio: 0.79; 95% confidence interval: 0.67, 0.92). In conclusion, the present study findings do not support recommendations for antioxidants supplementation to prevent all-cause, cancer, or non-cancer mortality on a population level. The significant inverse association between antioxidants use and respiratory disease mortality needs further study. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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15 pages, 1721 KiB

Open AccessArticle

Taurine Enhances Iron-Related Proteins and Reduces Lipid Peroxidation in Differentiated C2C12 Myotubes

by Ulrike Seidel, Kai Lüersen, Patricia Huebbe and Gerald Rimbach

Antioxidants 2020, 9(11), 1071; https://doi.org/10.3390/antiox9111071 - 31 Oct 2020

Cited by 7 | Viewed by 3000

Abstract

Taurine is a nonproteinogenic amino sulfonic acid in mammals. Interestingly, skeletal muscle is unable to synthesize taurine endogenously, and the processing of muscular taurine changes throughout ageing and under specific pathophysiological conditions, such as muscular dystrophy. Ageing and disease are also associated with [...] Read more.

Taurine is a nonproteinogenic amino sulfonic acid in mammals. Interestingly, skeletal muscle is unable to synthesize taurine endogenously, and the processing of muscular taurine changes throughout ageing and under specific pathophysiological conditions, such as muscular dystrophy. Ageing and disease are also associated with altered iron metabolism, especially when there is an excess of labile iron. The present study addresses the question of whether taurine connects cytoprotective effects and redox homeostasis in a previously unknown iron-dependent manner. Using cultured differentiated C2C12 myotubes, the impact of taurine on markers of lipid peroxidation, redox-sensitive enzymes and iron-related proteins was studied. Significant increases in the heme protein myoglobin and the iron storage protein ferritin were observed in response to taurine treatment. Taurine supplementation reduced lipid peroxidation and BODIPY oxidation by ~60 and 25%, respectively. Furthermore, the mRNA levels of redox-sensitive heme oxygenase (Hmox1), catalase (Cat) and glutamate-cysteine ligase (Gclc) and the total cellular glutathione content were lower in taurine-supplemented cells than they were in the control cells. We suggest that taurine may inhibit the initiation and propagation of lipid peroxidation by lowering basal levels of cellular stress, perhaps through reduction of the cellular labile iron pool. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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22 pages, 5134 KiB

Open AccessArticle

The Effect of Antioxidants on Photoreactivity and Phototoxic Potential of RPE Melanolipofuscin Granules from Human Donors of Different Age

by Magdalena M. Olchawa, Grzegorz M. Szewczyk, Andrzej C. Zadlo, Michal W. Sarna, Dawid Wnuk and Tadeusz J. Sarna

Antioxidants 2020, 9(11), 1044; https://doi.org/10.3390/antiox9111044 - 26 Oct 2020

Cited by 11 | Viewed by 2397

Abstract

One of the most prominent age-related changes of retinal pigment epithelium (RPE) is the accumulation of melanolipofuscin granules, which could contribute to oxidative stress in the retina. The purpose of this study was to determine the ability of melanolipofuscin granules from younger and [...] Read more.

One of the most prominent age-related changes of retinal pigment epithelium (RPE) is the accumulation of melanolipofuscin granules, which could contribute to oxidative stress in the retina. The purpose of this study was to determine the ability of melanolipofuscin granules from younger and older donors to photogenerate reactive oxygen species, and to examine if natural antioxidants could modify the phototoxic potential of this age pigment. Electron paramagnetic resonance (EPR) oximetry, EPR-spin trapping, and time-resolved detection of near-infrared phosphorescence were employed for measuring photogeneration of superoxide anion and singlet oxygen by melanolipofuscin isolated from younger and older human donors. Phototoxicity mediated by internalized melanolipofuscin granules with and without supplementation with zeaxanthin and α-tocopherol was analyzed in ARPE-19 cells by determining cell survival, oxidation of cellular proteins, organization of the cell cytoskeleton, and the cell specific phagocytic activity. Supplementation with antioxidants reduced aerobic photoreactivity and phototoxicity of melanolipofuscin granules. The effect was particularly noticeable for melanolipofuscin mediated inhibition of the cell phagocytic activity. Antioxidants decreased the extent of melanolipofuscin-dependent oxidation of cellular proteins and disruption of the cell cytoskeleton. Although melanolipofuscin might be involved in chronic phototoxicity of the aging RPE, natural antioxidants could partially ameliorate these harmful effects. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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16 pages, 2313 KiB

Open AccessArticle

Characterization of the Age-Dependent Changes in Antioxidant Defenses and Protein’s Sulfhydryl/Carbonyl Stress in Human Follicular Fluid

by Alice Luddi, Laura Governini, Angela Capaldo, Giovanna Campanella, Vincenzo De Leo, Paola Piomboni and Giuseppe Morgante

Antioxidants 2020, 9(10), 927; https://doi.org/10.3390/antiox9100927 - 28 Sep 2020

Cited by 11 | Viewed by 2438

Abstract

The oxidative stress, characterized by the imbalance between pro-oxidants and antioxidants molecules, seems to be involved in the pathogenesis of female subfertility. In particular, the presence of different markers of oxidative stress has been reported in human follicular fluid (FF) surrounding oocytes. Based [...] Read more.

The oxidative stress, characterized by the imbalance between pro-oxidants and antioxidants molecules, seems to be involved in the pathogenesis of female subfertility. In particular, the presence of different markers of oxidative stress has been reported in human follicular fluid (FF) surrounding oocytes. Based on its distinctive composition and on the close proximity to the oocyte, FF creates a unique microenvironment having a direct impact on oocyte quality, implantation, and early embryo development. An imbalance in reactive oxygen species (ROS) production in ovarian follicular fluid may have a negative effect on these processes and, as a consequence, on female fertility. Therefore, the aim of this study was to evaluate the redox state of the FF through various methodological approaches. By means of 2D-electrophoresis we demonstrated that the main structural changes occurring in the proteins of the follicular fluid of normovulatory women were correlated to the age of the patients and to the antioxidant defenses present in the FF. Measurement of these parameters could have clinical relevance, since the assessment of the oxidative stress rate may be helpful in evaluating in vitro fertilization potential. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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19 pages, 4744 KiB

Open AccessEditor’s ChoiceArticle

Anti-inflammatory and Anti-oxidant Activity of Hidrox^® in Rotenone-Induced Parkinson’s Disease in Mice

by Rosalba Siracusa, Maria Scuto, Roberta Fusco, Angela Trovato, Maria Laura Ontario, Roberto Crea, Rosanna Di Paola, Salvatore Cuzzocrea and Vittorio Calabrese

Antioxidants 2020, 9(9), 824; https://doi.org/10.3390/antiox9090824 - 03 Sep 2020

Cited by 104 | Viewed by 9030

Abstract

Background: In developed countries, the extension of human life is increasingly accompanied by a progressive increase in neurodegenerative diseases, most of which do not yet have effective therapy but only symptomatic treatments. In recent years, plant polyphenols have aroused considerable interest in the [...] Read more.

Background: In developed countries, the extension of human life is increasingly accompanied by a progressive increase in neurodegenerative diseases, most of which do not yet have effective therapy but only symptomatic treatments. In recent years, plant polyphenols have aroused considerable interest in the scientific community. The mechanisms currently hypothesized for the pathogenesis of Parkinson’s disease (PD) are neuroinflammation, oxidative stress and apoptosis. Hydroxytyrosol (HT), the main component of Hidrox^® (HD), has been shown to have some of the highest free radical evacuation and anti-inflammatory activities. Here we wanted to study the role of HD on the neurobiological and behavioral alterations induced by rotenone. Methods: A study was conducted in which mice received HD (10 mg/kg, i.p.) concomitantly with rotenone (5 mg/kg, o.s.) for 28 days. Results: Locomotor activity, catalepsy, histological damage and several characteristic markers of the PD, such as the dopamine transporter (DAT) content, tyrosine hydroxylase (TH) and accumulation of α-synuclein, have been evaluated. Moreover, we observed the effects of HD on oxidative stress, neuroinflammation, apoptosis and inflammasomes. Taken together, the results obtained highlight HD’s ability to reduce the loss of dopaminergic neurons and the damage associated with it by counteracting the three main mechanisms of PD pathogenesis. Conclusion: HD is subject to fewer regulations than traditional drugs to improve patients’ brain health and could represent a promising nutraceutical choice to prevent PD. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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15 pages, 3558 KiB

Open AccessArticle

SkQ1 Suppresses the p38 MAPK Signaling Pathway Involved in Alzheimer’s Disease-Like Pathology in OXYS Rats

by Natalia A. Muraleva, Natalia A. Stefanova and Nataliya G. Kolosova

Antioxidants 2020, 9(8), 676; https://doi.org/10.3390/antiox9080676 - 28 Jul 2020

Cited by 19 | Viewed by 2817

Abstract

Alzheimer’s disease (AD) is the most common type of dementia and is currently incurable, and mitogen-activated protein kinase (MAPK) p38 is implicated in the pathogenesis of AD. p38 MAPK inhibition is considered a promising strategy against AD, but there are no safe inhibitors [...] Read more.

Alzheimer’s disease (AD) is the most common type of dementia and is currently incurable, and mitogen-activated protein kinase (MAPK) p38 is implicated in the pathogenesis of AD. p38 MAPK inhibition is considered a promising strategy against AD, but there are no safe inhibitors capable of penetrating the blood–brain barrier. Earlier, we have shown that mitochondria-targeted antioxidant plastoquinonyl-decyltriphenylphosphonium (SkQ1) at nanomolar concentrations can prevent, slow down, or partially alleviate AD-like pathology in accelerated-senescence OXYS rats. Here we confirmed that dietary supplementation with SkQ1 during active progression of AD-like pathology in OXYS rats (aged 12–18 months) suppresses AD-like pathology progression, and for the first time, we showed that its effects are associated with suppression of p38 MAPK signaling pathway (MAPKsp) activity. Transcriptome analysis, western blotting, and immunofluorescent staining revealed that SkQ1 suppresses p38 MAPKsp activity in the hippocampus at the level of expression of genes involved in the p38 MAPKsp and reduces the phosphorylation of intermediate kinases (p38 MAPK and MK2) and a downstream protein (αB-crystallin). Thus, the anti-AD effects of SkQ1 are associated with improvement in the functioning of relevant signaling pathways and intracellular processes, thus making it a promising therapeutic agent for human AD. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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Review

Jump to: Research

28 pages, 817 KiB

Open AccessReview

Lipotoxic Impairment of Mitochondrial Function in β-Cells: A Review

by Axel Römer, Thomas Linn and Sebastian F. Petry

Antioxidants 2021, 10(2), 293; https://doi.org/10.3390/antiox10020293 - 15 Feb 2021

Cited by 17 | Viewed by 4195

Abstract

Lipotoxicity is a major contributor to type 2 diabetes mainly promoting mitochondrial dysfunction. Lipotoxic stress is mediated by elevated levels of free fatty acids through various mechanisms and pathways. Impaired peroxisome proliferator-activated receptor (PPAR) signaling, enhanced oxidative stress levels, and uncoupling of the [...] Read more.

Lipotoxicity is a major contributor to type 2 diabetes mainly promoting mitochondrial dysfunction. Lipotoxic stress is mediated by elevated levels of free fatty acids through various mechanisms and pathways. Impaired peroxisome proliferator-activated receptor (PPAR) signaling, enhanced oxidative stress levels, and uncoupling of the respiratory chain result in ATP deficiency, while β-cell viability can be severely impaired by lipotoxic modulation of PI3K/Akt and mitogen-activated protein kinase (MAPK)/extracellular-signal-regulated kinase (ERK) pathways. However, fatty acids are physiologically required for an unimpaired β-cell function. Thus, preparation, concentration, and treatment duration determine whether the outcome is beneficial or detrimental when fatty acids are employed in experimental setups. Further, ageing is a crucial contributor to β-cell decay. Cellular senescence is connected to loss of function in β-cells and can further be promoted by lipotoxicity. The potential benefit of nutrients has been broadly investigated, and particularly polyphenols were shown to be protective against both lipotoxicity and cellular senescence, maintaining the physiology of β-cells. Positive effects on blood glucose regulation, mitigation of oxidative stress by radical scavenging properties or regulation of antioxidative enzymes, and modulation of apoptotic factors were reported. This review summarizes the significance of lipotoxicity and cellular senescence for mitochondrial dysfunction in the pancreatic β-cell and outlines potential beneficial effects of plant-based nutrients by the example of polyphenols. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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20 pages, 568 KiB

Open AccessReview

Dietary Anti-Aging Polyphenols and Potential Mechanisms

by Jing Luo, Hongwei Si, Zhenquan Jia and Dongmin Liu

Antioxidants 2021, 10(2), 283; https://doi.org/10.3390/antiox10020283 - 13 Feb 2021

Cited by 86 | Viewed by 10289

Abstract

For years, the consumption of a diet rich in fruits and vegetables has been considered healthy, increasing longevity, and decreasing morbidities. With the assistance of basic research investigating the potential mechanisms, it has become clear that the beneficial effects of plant-based foods are [...] Read more.

For years, the consumption of a diet rich in fruits and vegetables has been considered healthy, increasing longevity, and decreasing morbidities. With the assistance of basic research investigating the potential mechanisms, it has become clear that the beneficial effects of plant-based foods are mainly due to the large amount of bioactive phenolic compounds contained. Indeed, substantial dietary intervention studies in humans have supported that the supplementation of polyphenols have various health-promoting effects, especially in the elderly population. In vitro examinations on the anti-aging mechanisms of polyphenols have been widely performed, using different types of natural and synthetic phenolic compounds. The aim of this review is to critically evaluate the experimental evidence demonstrating the beneficial effects of polyphenols on aging-related diseases. We highlight the potential anti-aging mechanisms of polyphenols, including antioxidant signaling, preventing cellular senescence, targeting microRNA, influencing NO bioavailability, and promoting mitochondrial function. While the trends on utilizing polyphenols in preventing aging-related disorders are getting growing attention, we suggest the exploration of the beneficial effects of the combination of multiple polyphenols or polyphenol-rich foods, as this would be more physiologically relevant to daily life. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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35 pages, 1837 KiB

Open AccessReview

Hydrogen Sulfide and Carnosine: Modulation of Oxidative Stress and Inflammation in Kidney and Brain Axis

by Vittorio Calabrese, Maria Scuto, Angela Trovato Salinaro, Giuseppe Dionisio, Sergio Modafferi, Maria Laura Ontario, Valentina Greco, Sebastiano Sciuto, Claus Peter Schmitt, Edward J. Calabrese and Verena Peters

Antioxidants 2020, 9(12), 1303; https://doi.org/10.3390/antiox9121303 - 18 Dec 2020

Cited by 36 | Viewed by 6416

Abstract

Emerging evidence indicates that the dysregulation of cellular redox homeostasis and chronic inflammatory processes are implicated in the pathogenesis of kidney and brain disorders. In this light, endogenous dipeptide carnosine (β-alanyl-L-histidine) and hydrogen sulfide (H₂S) exert cytoprotective actions through the modulation [...] Read more.

Emerging evidence indicates that the dysregulation of cellular redox homeostasis and chronic inflammatory processes are implicated in the pathogenesis of kidney and brain disorders. In this light, endogenous dipeptide carnosine (β-alanyl-L-histidine) and hydrogen sulfide (H₂S) exert cytoprotective actions through the modulation of redox-dependent resilience pathways during oxidative stress and inflammation. Several recent studies have elucidated a functional crosstalk occurring between kidney and the brain. The pathophysiological link of this crosstalk is represented by oxidative stress and inflammatory processes which contribute to the high prevalence of neuropsychiatric disorders, cognitive impairment, and dementia during the natural history of chronic kidney disease. Herein, we provide an overview of the main pathophysiological mechanisms related to high levels of pro-inflammatory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and neurotoxins, which play a critical role in the kidney–brain crosstalk. The present paper also explores the respective role of H₂S and carnosine in the modulation of oxidative stress and inflammation in the kidney–brain axis. It suggests that these activities are likely mediated, at least in part, via hormetic processes, involving Nrf2 (Nuclear factor-like 2), Hsp 70 (heat shock protein 70), SIRT-1 (Sirtuin-1), Trx (Thioredoxin), and the glutathione system. Metabolic interactions at the kidney and brain axis level operate in controlling and reducing oxidant-induced inflammatory damage and therefore, can be a promising potential therapeutic target to reduce the severity of renal and brain injuries in humans. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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25 pages, 605 KiB

Open AccessReview

Osteoprotective Roles of Green Tea Catechins

by Hsuan-Ti Huang, Tsung-Lin Cheng, Sung-Yen Lin, Cheng-Jung Ho, Joanna Y. Chyu, Rong-Sen Yang, Chung-Hwan Chen and Chwan-Li Shen

Antioxidants 2020, 9(11), 1136; https://doi.org/10.3390/antiox9111136 - 16 Nov 2020

Cited by 35 | Viewed by 5475

Abstract

Osteoporosis is the second most common disease only secondary to cardiovascular disease, with the risk of fracture increasing with age. Osteoporosis is caused by an imbalance between osteoblastogenesis and osteoclastogenesis processes. Osteoclastogenesis may be enhanced, osteoblastogenesis may be reduced, or both may be [...] Read more.

Osteoporosis is the second most common disease only secondary to cardiovascular disease, with the risk of fracture increasing with age. Osteoporosis is caused by an imbalance between osteoblastogenesis and osteoclastogenesis processes. Osteoclastogenesis may be enhanced, osteoblastogenesis may be reduced, or both may be evident. Inflammation and high reactive oxygen enhance osteoclastogenesis while reducing osteoblastogenesis by inducing osteoblast apoptosis and suppressing osteoblastic proliferation and differentiation. Catechins, the main polyphenols found in green tea with potent anti-oxidant and anti-inflammatory properties, can counteract the deleterious effects of the imbalance of osteoblastogenesis and osteoclastogenesis caused by osteoporosis. Green tea catechins can attenuate osteoclastogenesis by enhancing apoptosis of osteoclasts, hampering osteoclastogenesis, and prohibiting bone resorption in vitro. Catechin effects can be directly exerted on pre-osteoclasts/osteoclasts or indirectly exerted via the modulation of mesenchymal stem cells (MSCs)/stromal cell regulation of pre-osteoclasts through activation of the nuclear factor kB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) system. Catechins also can enhance osteoblastogenesis by enhancing osteogenic differentiation of MSCs and increasing osteoblastic survival, proliferation, differentiation, and mineralization. The in vitro effects of catechins on osteogenesis have been confirmed in several animal models, as well as in epidemiological observational studies on human subjects. Even though randomized control trials have not shown that catechins provide anti-fracture efficacy, safety data in the trials are promising. A large-scale, placebo-controlled, long-term randomized trial with a tea regimen intervention of optimal duration is required to determine anti-fracture efficacy. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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21 pages, 914 KiB

Open AccessReview

Dietary Antioxidants and the Mitochondrial Quality Control: Their Potential Roles in Parkinson’s Disease Treatment

by Davin Lee, Min Gu Jo, Seung Yeon Kim, Chang Geon Chung and Sung Bae Lee

Antioxidants 2020, 9(11), 1056; https://doi.org/10.3390/antiox9111056 - 28 Oct 2020

Cited by 9 | Viewed by 3376

Abstract

Advances in medicine and dietary standards over recent decades have remarkably increased human life expectancy. Unfortunately, the chance of developing age-related diseases, including neurodegenerative diseases (NDDs), increases with increased life expectancy. High metabolic demands of neurons are met by mitochondria, damage of which [...] Read more.

Advances in medicine and dietary standards over recent decades have remarkably increased human life expectancy. Unfortunately, the chance of developing age-related diseases, including neurodegenerative diseases (NDDs), increases with increased life expectancy. High metabolic demands of neurons are met by mitochondria, damage of which is thought to contribute to the development of many NDDs including Parkinson’s disease (PD). Mitochondrial damage is closely associated with the abnormal production of reactive oxygen species (ROS), which are widely known to be toxic in various cellular environments, including NDD contexts. Thus, ways to prevent or slow mitochondrial dysfunction are needed for the treatment of these NDDs. In this review, we first detail how ROS are associated with mitochondrial dysfunction and review the cellular mechanisms, such as the mitochondrial quality control (MQC) system, by which neurons defend against both abnormal production of ROS and the subsequent accumulation of damaged mitochondria. We next highlight previous studies that link mitochondrial dysfunction with PD and how dietary antioxidants might provide reinforcement of the MQC system. Finally, we discuss how aging plays a role in mitochondrial dysfunction and PD before considering how healthy aging through proper diet and exercise may be salutary. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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28 pages, 675 KiB

Open AccessReview

Impacts of Green Tea on Joint and Skeletal Muscle Health: Prospects of Translational Nutrition

by Hui-Ying Luk, Casey Appell, Ming-Chien Chyu, Chung-Hwan Chen, Chien-Yuan Wang, Rong-Sen Yang and Chwan-Li Shen

Antioxidants 2020, 9(11), 1050; https://doi.org/10.3390/antiox9111050 - 28 Oct 2020

Cited by 32 | Viewed by 9197

Abstract

Osteoarthritis and sarcopenia are two major joint and skeletal muscle diseases prevalent during aging. Osteoarthritis is a multifactorial progressive degenerative and inflammatory disorder of articular cartilage. Cartilage protection and pain management are the two most important strategies in the management of osteoarthritis. Sarcopenia, [...] Read more.

Osteoarthritis and sarcopenia are two major joint and skeletal muscle diseases prevalent during aging. Osteoarthritis is a multifactorial progressive degenerative and inflammatory disorder of articular cartilage. Cartilage protection and pain management are the two most important strategies in the management of osteoarthritis. Sarcopenia, a condition of loss of muscle mass and strength, is associated with impaired neuromuscular innervation, the transition of skeletal muscle fiber type, and reduced muscle regenerative capacity. Management of sarcopenia requires addressing both skeletal muscle quantity and quality. Emerging evidence suggests that green tea catechins play an important role in maintaining healthy joints and skeletal muscle. This review covers (i) the prevalence and etiology of osteoarthritis and sarcopenia, such as excessive inflammation and oxidative stress, mitochondrial dysfunction, and reduced autophagy; (ii) the effects of green tea catechins on joint health by downregulating inflammatory signaling mediators, upregulating anabolic mediators, and modulating miRNAs expression, resulting in reduced chondrocyte death, collagen degradation, and cartilage protection; (iii) the effects of green tea catechins on skeletal muscle health via maintaining a dynamic balance between protein synthesis and degradation and boosting the synthesis of mitochondrial energy metabolism, resulting in favorable muscle homeostasis and mitigation of muscle atrophy with aging; and (iv) the current study limitations and future research directions. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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24 pages, 1606 KiB

Open AccessReview

Nutrition and microRNAs: Novel Insights to Fight Sarcopenia

by Alessandra Barbiera, Laura Pelosi, Gigliola Sica and Bianca Maria Scicchitano

Antioxidants 2020, 9(10), 951; https://doi.org/10.3390/antiox9100951 - 02 Oct 2020

Cited by 16 | Viewed by 4189

Abstract

Sarcopenia is a progressive age-related loss of skeletal muscle mass and strength, which may result in increased physical frailty and a higher risk of adverse events. Low-grade systemic inflammation, loss of muscle protein homeostasis, mitochondrial dysfunction, and reduced number and function of satellite [...] Read more.

Sarcopenia is a progressive age-related loss of skeletal muscle mass and strength, which may result in increased physical frailty and a higher risk of adverse events. Low-grade systemic inflammation, loss of muscle protein homeostasis, mitochondrial dysfunction, and reduced number and function of satellite cells seem to be the key points for the induction of muscle wasting, contributing to the pathophysiological mechanisms of sarcopenia. While a range of genetic, hormonal, and environmental factors has been reported to contribute to the onset of sarcopenia, dietary interventions targeting protein or antioxidant intake may have a positive effect in increasing muscle mass and strength, regulating protein homeostasis, oxidative reaction, and cell autophagy, thus providing a cellular lifespan extension. MicroRNAs (miRNAs) are endogenous small non-coding RNAs, which control gene expression in different tissues. In skeletal muscle, a range of miRNAs, named myomiRNAs, are involved in many physiological processes, such as growth, development, and maintenance of muscle mass and function. This review aims to present and to discuss some of the most relevant molecular mechanisms related to the pathophysiological effect of sarcopenia. Besides, we explored the role of nutrition as a possible way to counteract the loss of muscle mass and function associated with ageing, with special attention paid to nutrient-dependent miRNAs regulation. This review will provide important information to better understand sarcopenia and, thus, to facilitate research and therapeutic strategies to counteract the pathophysiological effect of ageing. Full article

(This article belongs to the Special Issue Dietary Antioxidants for Modulating the Aging Processes)

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