International Journal of Molecular Sciences

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3 pages, 198 KiB

Open AccessEditorial

Nutrition and Aging

by M. Hasan Mohajeri

Int. J. Mol. Sci. 2023, 24(11), 9265; https://doi.org/10.3390/ijms24119265 - 25 May 2023

Cited by 2 | Viewed by 2278

Abstract

This Special Issue focuses on the importance of nutritional interventions for the delay of age-related conditions [...] Full article

(This article belongs to the Special Issue Nutrition and Aging)

Research

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18 pages, 1780 KiB

Open AccessArticle

Effects of Prolonged Dietary Curcumin Exposure on Skeletal Muscle Biochemical and Functional Responses of Aged Male Rats

by Candace N. Receno, Chen Liang, Donna L. Korol, Mustafa Atalay, Kevin S. Heffernan, Tom D. Brutsaert and Keith C. DeRuisseau

Int. J. Mol. Sci. 2019, 20(5), 1178; https://doi.org/10.3390/ijms20051178 - 7 Mar 2019

Cited by 37 | Viewed by 7282

Abstract

Oxidative stress resulting from decreased antioxidant protection and increased reactive oxygen and nitrogen species (RONS) production may contribute to muscle mass loss and dysfunction during aging. Curcumin is a phenolic compound shown to upregulate antioxidant defenses and directly quench RONS in vivo. This [...] Read more.

Oxidative stress resulting from decreased antioxidant protection and increased reactive oxygen and nitrogen species (RONS) production may contribute to muscle mass loss and dysfunction during aging. Curcumin is a phenolic compound shown to upregulate antioxidant defenses and directly quench RONS in vivo. This study determined the impact of prolonged dietary curcumin exposure on muscle mass and function of aged rats. Thirty-two-month-old male F344xBN rats were provided a diet with or without 0.2% curcumin for 4 months. The groups included: ad libitum control (CON; n = 18); 0.2% curcumin (CUR; n = 18); and pair-fed (PAIR; n = 18) rats. CUR rats showed lower food intake compared to CON, making PAIR a suitable comparison group. CUR rats displayed larger plantaris mass and force production (vs. PAIR). Nuclear fraction levels of nuclear factor erythroid-2 related-factor-2 were greater, and oxidative macromolecule damage was lower in CUR (vs. PAIR). There were no significant differences in measures of antioxidant status between any of the groups. No difference in any measure was observed between CUR and CON rats. Thus, consumption of curcumin coupled with reduced food intake imparted beneficial effects on aged skeletal muscle. The benefit of curcumin on aging skeletal muscle should be explored further. Full article

(This article belongs to the Special Issue Nutrition and Aging)

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21 pages, 5344 KiB

Open AccessArticle

Diabetes Impairs Angiogenesis and Induces Endothelial Cell Senescence by Up-Regulating Thrombospondin-CD47-Dependent Signaling

by Milad S. Bitar

Int. J. Mol. Sci. 2019, 20(3), 673; https://doi.org/10.3390/ijms20030673 - 4 Feb 2019

Cited by 36 | Viewed by 7187

Abstract

Endothelial dysfunction, impaired angiogenesis and cellular senescence in type 2 diabetes constitute dominant risk factors for chronic non-healing wounds and other cardiovascular disorders. Studying these phenomena in the context of diabetes and the TSP1-CD-47 signaling dictated the use of the in vitro wound [...] Read more.

Endothelial dysfunction, impaired angiogenesis and cellular senescence in type 2 diabetes constitute dominant risk factors for chronic non-healing wounds and other cardiovascular disorders. Studying these phenomena in the context of diabetes and the TSP1-CD-47 signaling dictated the use of the in vitro wound endothelial cultured system and an in vivo PVA sponge model of angiogenesis. Herein we report that diabetes impaired the in vivo sponge angiogenic capacity by decreasing cell proliferation, fibrovascular invasion and capillary density. In contrast, a heightened state of oxidative stress and elevated expression of TSP1 and CD47 both at the mRNA and protein levels were evident in this diabetic sponge model of wound healing. An in vitro culturing system involving wound endothelial cells confirmed the increase in ROS generation and the up-regulation of TSP1-CD47 signaling as a function of diabetes. We also provided evidence that diabetic wound endothelial cells (W-ECs) exhibited a characteristic feature that is consistent with cellular senescence. Indeed, enhanced SA-β-gal activity, cell cycle arrest, increased cell cycle inhibitors (CKIs) p53, p21 and p16 and decreased cell cycle promoters including Cyclin D1 and CDK4/6 were all demonstrated in these cells. The functional consequence of this cascade of events was illustrated by a marked reduction in diabetic endothelial cell proliferation, migration and tube formation. A genetic-based strategy in diabetic W-ECs using CD47 siRNA significantly ameliorated in these cells the excessiveness in oxidative stress, attenuation in angiogenic potential and more importantly the inhibition in cell cycle progression and its companion cellular senescence. To this end, the current data provide evidence linking the overexpression of TSP1-CD47 signaling in diabetes to a number of parameters associated with endothelial dysfunction including impaired angiogenesis, cellular senescence and a heightened state of oxidative stress. Moreover, it may also point to TSP1-CD47 as a potential therapeutic target in the treatment of the aforementioned pathologies. Full article

(This article belongs to the Special Issue Nutrition and Aging)

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16 pages, 2972 KiB

Open AccessArticle

Healthy Brain Aging Modifies Microglial Calcium Signaling In Vivo

by Maria Olmedillas del Moral, Nithi Asavapanumas, Néstor L. Uzcátegui and Olga Garaschuk

Int. J. Mol. Sci. 2019, 20(3), 589; https://doi.org/10.3390/ijms20030589 - 30 Jan 2019

Cited by 40 | Viewed by 4902

Abstract

Brain aging is characterized by a chronic, low-grade inflammatory state, promoting deficits in cognition and the development of age-related neurodegenerative diseases. Malfunction of microglia, the brain-resident immune cells, was suggested to play a critical role in neuroinflammation, but the mechanisms underlying this malfunctional [...] Read more.

Brain aging is characterized by a chronic, low-grade inflammatory state, promoting deficits in cognition and the development of age-related neurodegenerative diseases. Malfunction of microglia, the brain-resident immune cells, was suggested to play a critical role in neuroinflammation, but the mechanisms underlying this malfunctional phenotype remain unclear. Specifically, the age-related changes in microglial Ca²⁺ signaling, known to be linked to its executive functions, are not well understood. Here, using in vivo two-photon imaging, we characterize intracellular Ca²⁺ signaling and process extension of cortical microglia in young adult (2–4-month-old), middle-aged (9–11-month-old), and old (18–21-month-old) mice. Our data revealed a complex and nonlinear dependency of the properties of intracellular Ca²⁺ signals on an animal’s age. While the fraction of cells displaying spontaneous Ca²⁺ transients progressively increased with age, the frequencies and durations of the spontaneous Ca²⁺ transients followed a bell-shaped relationship, with the most frequent and largest Ca²⁺ transients seen in middle-aged mice. Moreover, in old mice microglial processes extending toward an ATP source moved faster but in a more disorganized manner, compared to young adult mice. Altogether, these findings identify two distinct phenotypes of aging microglia: a reactive phenotype, abundantly present in middle-aged animals, and a dysfunctional/senescent phenotype ubiquitous in old mice. Full article

(This article belongs to the Special Issue Nutrition and Aging)

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11 pages, 1862 KiB

Open AccessArticle

Hydrogen Indirectly Suppresses Increases in Hydrogen Peroxide in Cytoplasmic Hydroxyl Radical-Induced Cells and Suppresses Cellular Senescence

by Takahiro Sakai, Ryosuke Kurokawa, Shin-ichi Hirano and Jun Imai

Int. J. Mol. Sci. 2019, 20(2), 456; https://doi.org/10.3390/ijms20020456 - 21 Jan 2019

Cited by 16 | Viewed by 5670

Abstract

Bacteria inhabiting the human gut metabolize microbiota-accessible carbohydrates (MAC) contained in plant fibers and subsequently release metabolic products. Gut bacteria produce hydrogen (H₂), which scavenges the hydroxyl radical (•OH). Because H₂ diffuses within the cell, it is hypothesized that H [...] Read more.

Bacteria inhabiting the human gut metabolize microbiota-accessible carbohydrates (MAC) contained in plant fibers and subsequently release metabolic products. Gut bacteria produce hydrogen (H₂), which scavenges the hydroxyl radical (•OH). Because H₂ diffuses within the cell, it is hypothesized that H₂ scavenges cytoplasmic •OH (cyto •OH) and suppresses cellular senescence. However, the mechanisms of cyto •OH-induced cellular senescence and the physiological role of gut bacteria-secreted H₂ have not been elucidated. Based on the pyocyanin-stimulated cyto •OH-induced cellular senescence model, the mechanism by which cyto •OH causes cellular senescence was investigated by adding a supersaturated concentration of H₂ into the cell culture medium. Cyto •OH-generated lipid peroxide caused glutathione (GSH) and heme shortage, increased hydrogen peroxide (H₂O₂), and induced cellular senescence via the phosphorylation of ataxia telangiectasia mutated kinase serine 1981 (p-ATM^ser1981)/p53 serine 15 (p-p53^ser15)/p21 and phosphorylation of heme-regulated inhibitor (p-HRI)/phospho-eukaryotic translation initiation factor 2 subunit alpha serine 51 (p-eIF2α)/activating transcription factor 4 (ATF4)/p16 pathways. Further, H₂ suppressed increased H₂O₂ by suppressing cyto •OH-mediated lipid peroxide formation and cellular senescence induction via two pathways. H₂ produced by gut bacteria diffuses throughout the body to scavenge cyto •OH in cells. Therefore, it is highly likely that gut bacteria-produced H₂ is involved in intracellular maintenance of the redox state, thereby suppressing cellular senescence and individual aging. Hence, H₂ produced by intestinal bacteria may be involved in the suppression of aging. Full article

(This article belongs to the Special Issue Nutrition and Aging)

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13 pages, 3343 KiB

Open AccessArticle

Jowiseungchungtang Inhibits Amyloid-β Aggregation and Amyloid-β-Mediated Pathology in 5XFAD Mice

by Soo Jung Shin, Yu-on Jeong, Seong Gak Jeon, Sujin Kim, Seong-kyung Lee, Yunkwon Nam, Yong Ho Park, Dabi Kim, Youn Seok Lee, Hong Seok Choi, Jin-il Kim, Jwa-Jin Kim and Minho Moon

Int. J. Mol. Sci. 2018, 19(12), 4026; https://doi.org/10.3390/ijms19124026 - 13 Dec 2018

Cited by 10 | Viewed by 6459

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disease, which is accompanied by memory loss and cognitive dysfunction. Although a number of trials to treat AD are in progress, there are no drugs available that inhibit the progression of AD. As the aggregation of amyloid-β [...] Read more.

Alzheimer’s disease (AD) is a neurodegenerative disease, which is accompanied by memory loss and cognitive dysfunction. Although a number of trials to treat AD are in progress, there are no drugs available that inhibit the progression of AD. As the aggregation of amyloid-β (Aβ) peptides in the brain is considered to be the major pathology of AD, inhibition of Aβ aggregation could be an effective strategy for AD treatment. Jowiseungchungtang (JWS) is a traditional oriental herbal formulation that has been shown to improve cognitive function in patients or animal models with dementia. However, there are no reports examining the effects of JWS on Aβ aggregation. Thus, we investigated whether JWS could protect against both Aβ aggregates and Aβ-mediated pathology such as neuroinflammation, neurodegeneration, and impaired adult neurogenesis in 5 five familial Alzheimer’s disease mutations (5XFAD) mice, an animal model for AD. In an in vitro thioflavin T assay, JWS showed a remarkable anti-Aβ aggregation effect. Histochemical analysis indicated that JWS had inhibitory effects on Aβ aggregation, Aβ-induced pathologies, and improved adult hippocampal neurogenesis in vivo. Taken together, these results suggest the therapeutic possibility of JWS for AD targeting Aβ aggregation, Aβ-mediated neurodegeneration, and impaired adult hippocampal neurogenesis. Full article

(This article belongs to the Special Issue Nutrition and Aging)

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12 pages, 1971 KiB

Open AccessArticle

Oral Intake of Collagen Peptide Attenuates Ultraviolet B Irradiation-Induced Skin Dehydration In Vivo by Regulating Hyaluronic Acid Synthesis

by Min Cheol Kang, Silvia Yumnam and Sun Yeou Kim

Int. J. Mol. Sci. 2018, 19(11), 3551; https://doi.org/10.3390/ijms19113551 - 11 Nov 2018

Cited by 64 | Viewed by 10094

Abstract

Collagen peptide (CP) has beneficial effects on functions of the skin, such as skin barrier function and skin elasticity, in vivo. However, there are few studies investigating the mechanism underlying the potential effects of CP in skin epidermal moisturization after ultraviolet B (UVB) [...] Read more.

Collagen peptide (CP) has beneficial effects on functions of the skin, such as skin barrier function and skin elasticity, in vivo. However, there are few studies investigating the mechanism underlying the potential effects of CP in skin epidermal moisturization after ultraviolet B (UVB) irradiation. In this study, we examined whether orally-administered CP affects the loss of skin hydration induced by UVB irradiation in hairless mice. SKH-1 hairless mice were orally administered CP at two doses (500 and 1000 mg/kg) for nine weeks, and the dorsal skin was exposed to UVB. The potential effects of CP were evaluated by measuring the transepidermal water loss (TEWL), skin hydration, wrinkle formation, and hyaluronic acid expression in the dorsal mice skin. We found that oral administration of CP increased skin hydration and decreased wrinkle formation compared to the UVB-irradiated group. Treatment of CP increased the mRNA and protein expression of hyaluronic acid synthases (HAS-1 and -2) concomitant with an increased hyaluronic acid production in skin tissue. The expression of hyaluronidase (HYAL-1 and 2) mRNA was downregulated in the CP-treated group. In addition, the protein expression of skin-hydrating factors, filaggrin and involucrin, was upregulated via oral administration of CP. In summary, these results show that oral administration of CP increases hyaluronic acid levels, which decreases during UVB photoaging. Therefore, we suggest that CP can be used as a nutricosmetic ingredient with potential effects on UVB-induced skin dehydration and moisture loss in addition to wrinkle formation. Full article

(This article belongs to the Special Issue Nutrition and Aging)

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Review

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18 pages, 1120 KiB

Open AccessReview

Frailty, Cognitive Decline, Neurodegenerative Diseases and Nutrition Interventions

by María Elena Gómez-Gómez and Sara C. Zapico

Int. J. Mol. Sci. 2019, 20(11), 2842; https://doi.org/10.3390/ijms20112842 - 11 Jun 2019

Cited by 110 | Viewed by 13494

Abstract

Currently the human population is aging faster. This leads to higher dependency rates and the transformation of health and social care to adapt to this aged population. Among the changes developed by this population is frailty. It is defined as a clinically detectable [...] Read more.

Currently the human population is aging faster. This leads to higher dependency rates and the transformation of health and social care to adapt to this aged population. Among the changes developed by this population is frailty. It is defined as a clinically detectable syndrome, related to the aging of multiple physiological systems, which prompts a situation of vulnerability. The etiology of frailty seems to be multifactorial and its pathophysiology is influenced by the interaction of numerous factors. Morley et al. propose four main mechanisms triggering the frailty: atherosclerosis, sarcopenia, cognitive deterioration and malnutrition, with their respective metabolic alterations. Malnutrition is associated with cognitive impairment or functional loss, but it is also known that an inadequate nutritional status predisposes to cognitive frailty. Additionally, nutritional factors that may influence vascular risk factors will potentially have an effect on dementia decline among patients with cognitive frailty. This review aims to describe the nutritional factors that have been researched so far which may lead to the development of frailty, and especially cognitive decline. Full article

(This article belongs to the Special Issue Nutrition and Aging)

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20 pages, 803 KiB

Open AccessReview

Dietary Restriction and Neuroinflammation: A Potential Mechanistic Link

by Eugene Bok, Myungjin Jo, Shinrye Lee, Bo-Ram Lee, Jaekwang Kim and Hyung-Jun Kim

Int. J. Mol. Sci. 2019, 20(3), 464; https://doi.org/10.3390/ijms20030464 - 22 Jan 2019

Cited by 35 | Viewed by 6841

Abstract

Chronic neuroinflammation is a common feature of the aged brain, and its association with the major neurodegenerative changes involved in cognitive impairment and motor dysfunction is well established. One of the most potent antiaging interventions tested so far is dietary restriction (DR), which [...] Read more.

Chronic neuroinflammation is a common feature of the aged brain, and its association with the major neurodegenerative changes involved in cognitive impairment and motor dysfunction is well established. One of the most potent antiaging interventions tested so far is dietary restriction (DR), which extends the lifespan in various organisms. Microglia and astrocytes are two major types of glial cells involved in the regulation of neuroinflammation. Accumulating evidence suggests that the age-related proinflammatory activation of astrocytes and microglia is attenuated under DR. However, the molecular mechanisms underlying DR-mediated regulation of neuroinflammation are not well understood. Here, we review the current understanding of the effects of DR on neuroinflammation and suggest an underlying mechanistic link between DR and neuroinflammation that may provide novel insights into the role of DR in aging and age-associated brain disorders. Full article

(This article belongs to the Special Issue Nutrition and Aging)

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