scholarly journals Effects and Mechanisms of Resveratrol on Aging and Age-Related Diseases

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Dan-Dan Zhou ◽  
Min Luo ◽  
Si-Yu Huang ◽  
Adila Saimaiti ◽  
Ao Shang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factor ◽  
Chronic Diseases ◽  
Inflammatory Reaction ◽  
Mitochondrial Function ◽  
Red Wine ◽  
Life Extension ◽  
Age Related ◽  
Stress Relieving ◽  
Prevention And Treatment

The aging of population has become an issue of great concern because of its rapid increase. Aging is an important risk factor of many chronic diseases. Resveratrol could be found in many foods, such as grapes, red wine, peanuts, and blueberries. Many studies reported that resveratrol possessed various bioactivities, such as antioxidant, anti-inflammatory, cardiovascular protection, anticancer, antidiabetes mellitus, antiobesity, neuroprotection, and antiaging effects. The antiaging mechanisms of resveratrol were mainly ameliorating oxidative stress, relieving inflammatory reaction, improving mitochondrial function, and regulating apoptosis. Resveratrol could be an effective and safe compound for the prevention and treatment of aging and age-related diseases. In this review, we summarize the effects of resveratrol on aging, life extension, and several age-related diseases, with special attention paid to the mechanisms of antiaging action.

scholarly journals Disparate Central and Peripheral Effects of Circulating IGF-1 Deficiency on Tissue Mitochondrial Function

2019 ◽  
Vol 57 (3) ◽  
pp. 1317-1331 ◽  
Author(s):  
Gavin Pharaoh ◽  
Daniel Owen ◽  
Alexander Yeganeh ◽  
Pavithra Premkumar ◽  
Julie Farley ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Spatial Learning ◽  
Mitochondrial Function ◽  
Coupling Efficiency ◽  
Redox Status ◽  
Cellular Aging ◽  
Age Related ◽  
The Brain ◽  
Circulating Levels

AbstractAge-related decline in circulating levels of insulin-like growth factor (IGF)-1 is associated with reduced cognitive function, neuronal aging, and neurodegeneration. Decreased mitochondrial function along with increased reactive oxygen species (ROS) and accumulation of damaged macromolecules are hallmarks of cellular aging. Based on numerous studies indicating pleiotropic effects of IGF-1 during aging, we compared the central and peripheral effects of circulating IGF-1 deficiency on tissue mitochondrial function using an inducible liver IGF-1 knockout (LID). Circulating levels of IGF-1 (~ 75%) were depleted in adult male Igf1f/f mice via AAV-mediated knockdown of hepatic IGF-1 at 5 months of age. Cognitive function was evaluated at 18 months using the radial arm water maze and glucose and insulin tolerance assessed. Mitochondrial function was analyzed in hippocampus, muscle, and visceral fat tissues using high-resolution respirometry O2K as well as redox status and oxidative stress in the cortex. Peripherally, IGF-1 deficiency did not significantly impact muscle mass or mitochondrial function. Aged LID mice were insulin resistant and exhibited ~ 60% less adipose tissue but increased fat mitochondrial respiration (20%). The effects on fat metabolism were attributed to increases in growth hormone. Centrally, IGF-1 deficiency impaired hippocampal-dependent spatial acquisition as well as reversal learning in male mice. Hippocampal mitochondrial OXPHOS coupling efficiency and cortex ATP levels (~ 50%) were decreased and hippocampal oxidative stress (protein carbonylation and F2-isoprostanes) was increased. These data suggest that IGF-1 is critical for regulating mitochondrial function, redox status, and spatial learning in the central nervous system but has limited impact on peripheral (liver and muscle) metabolism with age. Therefore, IGF-1 deficiency with age may increase sensitivity to damage in the brain and propensity for cognitive deficits. Targeting mitochondrial function in the brain may be an avenue for therapy of age-related impairment of cognitive function. Regulation of mitochondrial function and redox status by IGF-1 is essential to maintain brain function and coordinate hippocampal-dependent spatial learning. While a decline in IGF-1 in the periphery may be beneficial to avert cancer progression, diminished central IGF-1 signaling may mediate, in part, age-related cognitive dysfunction and cognitive pathologies potentially by decreasing mitochondrial function.

scholarly journals Advances on antioxidants in research and applications

2019 ◽  
Vol 131 ◽  
pp. 01009
Author(s):  
Ruirui Song ◽  
Qi Wu ◽  
Lin Zhao ◽  
Zhenyu Yun
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Chronic Diseases ◽  
Significant Role ◽  
Human Body ◽  
Relevant Research ◽  
Redox Equilibrium ◽  
Practical Applications ◽  
Existing Problems ◽  
Prevention And Treatment

Antioxidants play a significant role in the prevention and treatment of numerous chronic diseases as they prevent oxidative stress and maintain reduction-oxidation (redox) equilibrium in the human body by eliminating reactive free radicals effectively. This study focused on the types and applications of antioxidants and discussed the existing problems with regard to the practical applications of antioxidants. Also, it presented a review of the latest research on antioxidants in China and abroad and performed a comprehensive, objective analysis of relevant research on antioxidants.

scholarly journals Rationale for Antioxidant Supplementation in Sarcopenia

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Francesco Cerullo ◽  
Giovanni Gambassi ◽  
Matteo Cesari
Keyword(s):  
Oxidative Stress ◽  
Muscle Function ◽  
Molecular Mechanisms ◽  
Motor Units ◽  
Oxygen Species ◽  
Antioxidant Supplementation ◽  
Present Evidence ◽  
Progressive Loss ◽  
Age Related ◽  
Prevention And Treatment

Sarcopenia is an age-related clinical condition characterized by the progressive loss of motor units and wasting of muscle fibers resulting in decreased muscle function. The molecular mechanisms leading to sarcopenia are not completely identified, but the increased oxidative damage occurring in muscle cells during the course of aging represents one of the most accepted underlying pathways. In fact, skeletal muscle is a highly oxygenated tissue and the generation of reactive oxygen species is particularly enhanced in both contracting and at rest conditions. It has been suggested that oral antioxidant supplementation may contribute at reducing indices of oxidative stress both in animal and human models by reinforcing the natural endogenous defenses. Aim of the present paper is to discuss present evidence related to possible benefits of oral antioxidants in the prevention and treatment of sarcopenia.

Red wine extract protects against oxidative-stress-induced endothelial senescence

2012 ◽  
Vol 123 (8) ◽  
pp. 499-507 ◽  
Author(s):  
Ilse P. G. Botden ◽  
Hisko Oeseburg ◽  
Matej Durik ◽  
Frank P. J. Leijten ◽  
Leonie C. Van Vark-Van Der Zee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Red Wine ◽  
Umbilical Vein ◽  
Critical Role ◽  
Sirtuin 1 ◽  
Mrna Levels ◽  
Nitric Oxide Synthase Inhibitor ◽  
Age Related ◽  
Cox 2

Red wine polyphenols may preserve endothelial function during aging. Endothelial cell senescence enhances age-related endothelial dysfunction. We investigated whether RWE (red wine extract) prevents oxidative-stress-induced senescence in HUVECs (human umbilical-vein endothelial cells). Senescence was induced by exposing HUVECs to tBHP (t-butylhydroperoxide), and quantified by senescence-associated β-galactosidase staining. RWE (0–50 μg/ml) concentration dependently decreased senescence by maximally 33±7.1%. RWE prevented the senescence-associated increase in p21 protein expression, inhibited tBHP-induced DNA damage of endothelial cells and induced relaxation of PCAs (porcine coronary arteries). Inhibition of SIRT1 (sirtuin 1) by sirtinol partially reversed the effect of RWE on tBHP-induced senescence, whereas both the NOS (nitric oxide synthase) inhibitor L-NMMA (NG-monomethyl-L-arginine) and the COX (cyclo-oxygenase) inhibitor indomethacin fully inhibited it. Furthermore, incubation of HUVECs with RWE increased eNOS (endothelial NOS) and COX-2 mRNA levels as well as phosphorylation of eNOS at Ser1177. RWE protects endothelial cells from tBHP-induced senescence. NO and COX-2, in addition to activation of SIRT1, play a critical role in the inhibition of senescence induction in human endothelial cells by RWE.

scholarly journals Implication of Hyperhomocysteinemia in Blood Retinal Barrier (BRB) Dysfunction

Biomolecules ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 1119 ◽  
Author(s):  
Amany Tawfik ◽  
Yara A. Samra ◽  
Nehal M. Elsherbiny ◽  
Mohamed Al-Shabrawey
Keyword(s):  
Oxidative Stress ◽  
Risk Factor ◽  
Vision Loss ◽  
Neurological Diseases ◽  
Brain Inflammation ◽  
Age Related Macular Degeneration ◽  
Matrix Remodeling ◽  
Blood Retinal Barrier ◽  
Age Related

Elevated plasma homocysteine (Hcy) level, known as hyperhomocysteinemia (HHcy) has been linked to different systemic and neurological diseases, well-known as a risk factor for systemic atherosclerosis and cardiovascular disease (CVD) and has been identified as a risk factor for several ocular disorders, such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). Different mechanisms have been proposed to explain HHcy-induced visual dysfunction, including oxidative stress, upregulation of inflammatory mediators, retinal ganglion cell apoptosis, and extracellular matrix remodeling. Our previous studies using in vivo and in vitro models of HHcy have demonstrated that Hcy impairs the function of both inner and outer blood retinal barrier (BRB). Dysfunction of BRB is a hallmark of vision loss in DR and AMD. Our findings highlighted oxidative stress, ER stress, inflammation, and epigenetic modifications as possible mechanisms of HHcy-induced BRB dysfunction. In addition, we recently reported HHcy-induced brain inflammation as a mechanism of blood–brain barrier (BBB) dysfunction and pathogenesis of Alzheimer’s disease (AD). Moreover, we are currently investigating the activation of glutamate receptor N-methyl-d-aspartate receptor (NMDAR) as the molecular mechanism for HHcy-induced BRB dysfunction. This review focuses on the studied effects of HHcy on BRB and the controversial role of HHcy in the pathogenesis of aging neurological diseases such as DR, AMD, and AD. We also highlight the possible mechanisms for such deleterious effects of HHcy.

scholarly journals Amla Enhances Mitochondrial Spare Respiratory Capacity by Increasing Mitochondrial Biogenesis and Antioxidant Systems in a Murine Skeletal Muscle Cell Line

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Hirotaka Yamamoto ◽  
Katsutaro Morino ◽  
Lemecha Mengistu ◽  
Taishi Ishibashi ◽  
Kohei Kiriyama ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Cell ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Skeletal Muscle Cell ◽  
Antioxidant Systems ◽  
Respiratory Capacity ◽  
Age Related ◽  
Murine Skeletal Muscle

Amla is one of the most important plants in Indian traditional medicine and has been shown to improve various age-related disorders while decreasing oxidative stress. Mitochondrial dysfunction is a proposed cause of aging through elevated oxidative stress. In this study, we investigated the effects of Amla on mitochondrial function in C2C12 myotubes, a murine skeletal muscle cell model with abundant mitochondria. Based on cell flux analysis, treatment with an extract of Amla fruit enhanced mitochondrial spare respiratory capacity, which enables cells to overcome various stresses. To further explore the mechanisms underlying these effects on mitochondrial function, we analyzed mitochondrial biogenesis and antioxidant systems, both proposed regulators of mitochondrial spare respiratory capacity. We found that Amla treatment stimulated both systems accompanied by AMPK and Nrf2 activation. Furthermore, we found that Amla treatment exhibited cytoprotective effects and lowered reactive oxygen species (ROS) levels in cells subjected to t-BHP-induced oxidative stress. These effects were accompanied by increased oxygen consumption, suggesting that Amla protected cells against oxidative stress by using enhanced spare respiratory capacity to produce more energy. Thus we identified protective effects of Amla, involving activation of mitochondrial function, which potentially explain its various effects on age-related disorders.

scholarly journals Anthocyanins and Human Health—A Focus on Oxidative Stress, Inflammation and Disease

Antioxidants ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 366 ◽  
Author(s):  
Hollie Speer ◽  
Nathan M. D’Cunha ◽  
Natalie I. Alexopoulos ◽  
Andrew J. McKune ◽  
Nenad Naumovski
Keyword(s):  
Oxidative Stress ◽  
Treatment Strategies ◽  
Food Sources ◽  
Cardiometabolic Health ◽  
Physiological Effects ◽  
Beneficial Effects ◽  
Age Related ◽  
The Everyday ◽  
Prevention And Treatment ◽  
Apoptotic Effects

Consumption of anthocyanins (ACNs), due to their antioxidant, anti-inflammatory and anti-apoptotic effects, has been proposed for the prevention and treatment of several different diseases and conditions. ACNs are recognized as one of the leading nutraceuticals for prolonging health benefits through the attenuation of oxidative stress, and inflammatory or age-related diseases. Increased consumption of ACNs has the potential to attenuate the damage ensuing from oxidative stress, inflammation, enhance cardiometabolic health, and delay symptoms in predisposed neuropathology. A myriad of evidence supports ACN consumption as complementary or standalone treatment strategies for non-communicable diseases (NCDs) including obesity, diabetes, cardiovascular disease (CVD), neurodegenerative diseases, as well as, more recently, for the modulation of gut bacteria and bone metabolism. While these findings indicate the beneficial effects of ACN consumption, their food sources differ vastly in ACN composition and thus potentially in their physiological effects. Consumption of foods high in ACNs can be recommended for their potential beneficial health effects due to their relatively easy and accessible addition to the everyday diet.

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