scholarly journals Bifidobacterium adolescentis improves lifespan and healthspan by regulating catalase activity and oxidative stress-associated metabolites

2020 ◽  
Author(s):  
Shujie Chen ◽  
Luyi Chen ◽  
Yadong Qi ◽  
Jilei Xu ◽  
Qiwei Ge ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Catalase Activity ◽  
Fecal Microbiota ◽  
Bifidobacterium Adolescentis ◽  
C Elegans ◽  
Host Interaction ◽  
Age Related ◽  
Ros Accumulation ◽  
Gut Microbial Community ◽  
Host Metabolism

Abstract Microbiota-host interaction was involved in aging, while the specific bacterium was undetermined. To identify candidate bacterium with aging, we performed fecal microbiota sequencing. Less richness of gut microbial community, and a reduction of B.adolescentis abundance was observed in elderly individuals. B. adolescentis supplement improved osteoporosis and neurodegeneration in telomerase RNA component deletion (Terc−/−) aged mice. B.adolescentis induced prolongevity and healthspan improvement in Drosophila melanogaster and C. elegans. Transgenic deletion of ctl-2 in C. elegans abolished the effect on lifespan and healthspan by B. adolescentis. The catalase activity was decreased in skeletal muscle and brain tissues of Terc−/− mice, as well as cellular senescence in mouse embryonic fibroblasts. B. adolescentis alleviated ROS accumulation by regulation of oxidative stress-associated metabolites. These results suggest a role for B. adolescentis in improving lifespan and healthspan by regulating catalase activity and host metabolism. Supplement with commensal bacteria is a promising strategy against age related diseases.

scholarly journals The Redox System inC. elegans, a Phylogenetic Approach

2012 ◽  
Vol 2012 ◽  
pp. 1-20 ◽  
Author(s):  
Andrew D. Johnston ◽  
Paul R. Ebert
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Cellular Damage ◽  
Future Research ◽  
Homologous Proteins ◽  
Redox Biology ◽  
Redox Signalling ◽  
C Elegans ◽  
Age Related

Oxidative stress is a toxic state caused by an imbalance between the production and elimination of reactive oxygen species (ROS). ROS cause oxidative damage to cellular components such as proteins, lipids, and nucleic acids. While the role of ROS in cellular damage is frequently all that is noted, ROS are also important in redox signalling. The “Redox Hypothesis" has been proposed to emphasize a dual role of ROS. This hypothesis suggests that the primary effect of changes to the redox state is modified cellular signalling rather than simply oxidative damage. In extreme cases, alteration of redox signalling can contribute to the toxicity of ROS, as well as to ageing and age-related diseases. The nematode speciesCaenorhabditis elegansprovides an excellent model for the study of oxidative stress and redox signalling in animals. We use protein sequences from central redox systems inHomo sapiens,Drosophila melanogaster, andSaccharomyces cerevisiaeto query Genbank for homologous proteins inC. elegans. We then use maximum likelihood phylogenetic analysis to compare protein families betweenC. elegansand the other organisms to facilitate future research into the genetics of redox biology.

scholarly journals Mitochondrial sirtuins sir-2.2 and sir-2.3 regulate lifespan in C. elegans

2017 ◽  
Author(s):  
Sarah M. Chang ◽  
Melanie R. McReynolds ◽  
Wendy Hanna-Rose
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Drug Targets ◽  
Physiological Role ◽  
Oxidative Stress Response ◽  
Altered Expression ◽  
C Elegans ◽  
Mitochondrial Superoxide ◽  
Age Related ◽  
Extended Lifespan

ABSTRACTMitochondrial sirtuins regulate biochemical pathways and are emerging drug targets for metabolic and age-related diseases such as cancer, diabetes, and neurodegeneration. Yet, their functions remain unclear. Here, we uncover a novel physiological role for the C. elegans mitochondrial sirtuins, sir-2.2 and sir-2.3, in lifespan regulation. Using a genetic approach, we demonstrate that sir-2.2 and sir-2.3 mutants live 28-30% longer than controls when fed the normal lab diet of E. coli OP50. Interestingly, this effect is diet specific and is not observed when animals are fed the strain HT115, which is typically used for RNAi experiments. While decreased consumption of food is a known mechanism for lifespan extension, this does not account for the increased lifespan in the mitochondrial sirtuin mutants. sir-2.2 and sir-2.3 mutants display altered expression of genes involved in oxidative stress response, including increased expression of the mitochondrial superoxide dismutase sod-3 and decreased levels of catalases ctl-1 and ctl-2. Like their extended lifespan phenotype, these alterations in oxidative stress gene expression are diet dependent. The mitochondrial sirtuin mutants are more resistant to the lifespan extending effects of low levels of superoxide, suggesting that their increased lifespan involves a hormetic response. Our data suggest that sir-2.2 and sir-2.3 are not completely redundant in function and may possess overlapping yet distinct mechanisms for regulating oxidative stress response and lifespan.

scholarly journals Fisetin Rescues the Mice Brains Against D-Galactose-Induced Oxidative Stress, Neuroinflammation and Memory Impairment

2021 ◽  
Vol 12 ◽  
Author(s):  
Sareer Ahmad ◽  
Amjad Khan ◽  
Waqar Ali ◽  
Myeung Hoon Jo ◽  
Junsung Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurological Disorders ◽  
Memory Impairment ◽  
Neurological Impairment ◽  
Oxygen Species ◽  
Protective Effects ◽  
Age Related ◽  
Ros Accumulation ◽  
Anti Oxidant ◽  
Antioxidant Effects

Herein, we have evaluated the protective potentials of Fisetin against d-galactose-induced oxidative stress, neuroinflammation, and memory impairment in mice. d-galactose (D-gal) causes neurological impairment by inducing reactive oxygen species (ROS), neuroinflammation, and synaptic dysfunction, whereas fisetin (Fis) is a natural flavonoid having potential antioxidant effects, and has been used against different models of neurodegenerative diseases. Here, the normal mice were injected with D-gal (100 mg/kg/day for 60 days) and fisetin (20 mg/kg/day for 30 days). To elucidate the protective effects of fisetin against d-galactose induced oxidative stress-mediated neuroinflammation, we conducted western blotting, biochemical, behavioral, and immunofluorescence analyses. According to our findings, D-gal induced oxidative stress, neuroinflammation, synaptic dysfunctions, and cognitive impairment. Conversely, Fisetin prevented the D-gal-mediated ROS accumulation, by regulating the endogenous anti-oxidant mechanisms, such as Sirt1/Nrf2 signaling, suppressed the activated p-JNK/NF-kB pathway, and its downstream targets, such as inflammatory cytokines. Hence, our results together with the previous reports suggest that Fisetin may be beneficial in age-related neurological disorders.

Anti-aging and Anti-aggregation Properties of Polyphenolic Compounds in C. elegans

2018 ◽  
Vol 24 (19) ◽  
pp. 2107-2120 ◽  
Author(s):  
Nikoletta Papaevgeniou ◽  
Niki Chondrogianni
Keyword(s):  
Oxidative Stress ◽  
Model Organism ◽  
Protective Role ◽  
Polyphenolic Compounds ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Beneficial Effects ◽  
Age Related ◽  
Anti Oxidant ◽  
Main Model

Polyphenols constitute a group of compounds that have been highly investigated for their beneficial effects against various pathologic and non-pathologic conditions and diseases. Among their multi-faceted properties, their anti-oxidant potential nominates them as ideal protective candidates for conditions characterized by elevated levels of oxidative stress, including aging and age-related diseases. The nematode Caenorhabditis elegans is a multicellular model organism that is highly exploited in studies related to aging and age-associated pathologies. In this review, we will summarize studies where polyphenolic compounds have been tested for their anti-aging potential and their protective role against the progression of age-related diseases using C. elegans as their main model.

scholarly journals Serine Deficiency Exacerbates Inflammation and Oxidative Stress via Microbiota-Gut-Brain Axis in D-Galactose-Induced Aging Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Fengen Wang ◽  
Hongbin Zhou ◽  
Ligang Deng ◽  
Lei Wang ◽  
Jingqing Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Short Chain Fatty Acid ◽  
Inflammatory Responses ◽  
Basal Diet ◽  
Fecal Microbiota ◽  
Defense System ◽  
Age Related ◽  
The Brain ◽  
And Oxidative Stress ◽  
Microbiota Diversity

Inflammation and oxidative stress play key roles in the process of aging and age-related diseases. Since serine availability plays important roles in the support of antioxidant and anti-inflammatory defense system, we explored whether serine deficiency affects inflammatory and oxidative status in D-galactose-induced aging mice. Male mice were randomly assigned into four groups: mice fed a basal diet, mice fed a serine- and glycine-deficient (SGD) diet, mice injected with D-galactose and fed a basal diet, and mice injected with D-galactose and fed an SGD diet. The results showed that D-galactose resulted in oxidative and inflammatory responses, while serine deficiency alone showed no such effects. However, serine deficiency significantly exacerbated oxidative stress and inflammation in D-galactose-treated mice. The composition of fecal microbiota was affected by D-galactose injection, which was characterized by decreased microbiota diversity and downregulated ratio of Firmicutes/Bacteroidetes, as well as decreased proportion of Clostridium XIVa. Furthermore, serine deficiency exacerbated these changes. Additionally, serine deficiency in combination with D-galactose injection significantly decreased fecal butyric acid content and gene expression of short-chain fatty acid transporters (Slc16a3 and Slc16a7) and receptor (Gpr109a) in the brain. Finally, serine deficiency exacerbated the decrease of expression of phosphorylated AMPK and the increase of expression of phosphorylated NFκB p65, which were caused by D-galactose injection. In conclusion, our results suggested that serine deficiency exacerbated inflammation and oxidative stress in D-galactose-induced aging mice. The involved mechanisms might be partially attributed to the changes in the microbiota-gut-brain axis affected by serine deficiency.

scholarly journals Ghrelin Protects Human Lens Epithelial Cells against Oxidative Stress-Induced Damage

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Jie Bai ◽  
Fan Yang ◽  
Li Dong ◽  
Yi Zheng
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Human Lens ◽  
Morphological Examination ◽  
Important Mediator ◽  
Age Related ◽  
Ros Accumulation ◽  
Cellular Apoptosis ◽  
Antioxidant Supplements

Oxidative stress has been recognized as an important mediator in the pathogenesis of age-related cataracts; using antioxidant supplements is one plausible strategy to protect the antioxidative defense system against oxidative stress. Ghrelin administration is expected to reduce ROS, preventing the onset of different diseases. The role of ghrelin, if any, in protecting against oxidative stress in HLECs has never been examined. In the present study, we investigated the effects of ghrelin against H2O2-induced oxidative stress and the associated molecular mechanisms in HLECs and rat lenses. The results showed that pretreatment with ghrelin reduced H2O2-induced cellular apoptosis and ROS accumulation, increased the expression levels of SOD and CAT, and decreased the expression level of MDA. The morphological examination showed that the ghrelin-treated lens organ culture maintained transparency. This is the first report to show that ghrelin can protect HLECs from H2O2-induced oxidative stress. Our findings suggest that ghrelin may prevent the progression of cataracts, which has treatment value for ophthalmologists.

scholarly journals Bifidobacterium adolescentis regulates catalase activity and host metabolism and improves healthspan and lifespan in multiple species

Nature Aging ◽  
2021 ◽  
Vol 1 (11) ◽  
pp. 991-1001
Author(s):  
Shujie Chen ◽  
Luyi Chen ◽  
Yadong Qi ◽  
Jilei Xu ◽  
Qiwei Ge ◽  
...  
Keyword(s):  
Catalase Activity ◽  
Bifidobacterium Adolescentis ◽  
Multiple Species ◽  
Host Metabolism

scholarly journals Carnosol Improved Lifespan and Healthspan by Promoting Antioxidant Capacity in Caenorhabditis elegans

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Chunxiu Lin ◽  
Xiaoying Zhang ◽  
Zuanxian Su ◽  
Jie Xiao ◽  
Muwen Lv ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Stress Condition ◽  
Natural Antioxidants ◽  
Antioxidant Enzyme Activities ◽  
Good Source ◽  
Oxidative Stress Condition ◽  
C Elegans ◽  
Ros Accumulation ◽  
Mda Content

Carnosol, a phenolic diterpene, is one of the main constituents of Rosmarinus. It is known to possess a range of bioactivities, including antioxidant, anticancer, antimicrobial, and anti-inflammatory properties. Nevertheless, the antiaging effects of carnosol have received little attention. This study first indicated that carnosol increased the healthspan of Caenorhabditis elegans (C. elegans). First, compared with the control condition, carnosol treatment effectively decreased ROS accumulation under normal or oxidative stress condition, significantly increased several key antioxidant enzyme activities, and significantly decreased MDA content. Second, carnosol effectively prolonged lifespan under normal and stress conditions and slowed aging-related declines, including mobility, age pigmentation, and neurodegenerative disease, but had no effect on fertility and fat deposition. Finally, carnosol-mediated longevity required the upregulated expression of sod-3, sod-5, hsf-1, hsp-16.1, and hsp-16.2 and was dependent on the hsf-1 gene. Increased DAF-16 translocation was observed, but daf-16 was independent of the effects on lifespan induced by carnosol. These results suggested that carnosol might serve as a good source of natural antioxidants, and in particular, carnosol could be explored as a potential dietary supplement to slow aging.

Eugenol Elicits Prolongevity by Increasing Resistance to Oxidative Stress in C. elegans

2021 ◽  
Vol 20 ◽  
Author(s):  
Nikhat Parween ◽  
Amber Jabeen ◽  
Birendra Prasad
Keyword(s):  
Oxidative Stress ◽  
Animal Model ◽  
Caenorhabditis Elegans ◽  
Ocimum Sanctum ◽  
Human Consumption ◽  
C Elegans ◽  
Slowing Down ◽  
Age Related ◽  
Mutant Strains ◽  
Therapeutic Compound

Aim: To analyze the efficacy of eugenol on longevity by assessing its antioxidant effect using Caenorhabditis elegans as an animal model. Background: Eugenol is a major polyphenolic component of Ocimum sanctum (Tulsi) which attributes wide pharmacological activities and can serve as a biomarker. However, the possible effect of eugenol on longevity in Caenorhabditis elegans has not been reported. Objective: The objective of this investigation was to provide first scientific based results about effect of eugenol on longevity, slowing down of paralysis in Alzheimer’s model and mechanism behind it in Caenorhabditis elegans animal model system. Results: Extract of Ocimum sanctumand eugenol increased lifespan and provided indemnity against pro-oxidants. It also significantly improved healthy ageing and slowed the progression of neurodegeneration in CL4176 Alzheimer’s model of worm by increasing survival against prooxidants and slowing down the paralysis. Longevity effect was independent of the DAF-16 as observed by using DAF-16::GFP and daf-16 null mutant strains. These results implicate eugenol as a potent therapeutic compound which may curtail ageing and age related disorders like- Alzheimer’s disease. Conclusion: The present work demonstrated eugenol as a potential anti-ageing compound which may curtail ageing, improve heath span by enhancing resistance to oxidative stress and exerts its effect independent of DAF-16 pathway. So, it can be assumed that eugenol can be beneficial to humans as well, albeit further research is necessary before declaring it for human consumption.

scholarly journals RME-1 is required for lifespan extension and increased resistance to stresses associated with decreased insulin/IGF-1-like signaling in Caenorhabditis elegans

2017 ◽  
Vol 69 (3) ◽  
pp. 417-425
Author(s):  
Chul-Kyu Kim ◽  
Sang-Kyu Park
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Growth Factor ◽  
Heat Shock ◽  
Aging Effect ◽  
Lifespan Extension ◽  
Genetic Pathway ◽  
C Elegans ◽  
Age Related ◽  
Underlying Mechanisms

The insulin/insulin-like growth factor (IGF)-1 signaling (IIS) pathway is a conserved life span-modulating genetic pathway. Many genes involved in lifespan extension associated with decreased signaling of the IIS pathway have been identified. In the present study, we found a novel gene required for the effect of the IIS pathway on the stress response and aging in C. elegans. Receptor mediated endocytosis (RME)-1 is expressed ubiquitously and known to be involved in cellular endocytic transport. Knockdown of rme-1abolished the lifespan-extending effect caused by decreased IIS. In addition, resistance to oxidative stress, heat shock and ultraviolet irradiation were significantly decreased when the expression of RME-1 was blocked. The delayed age-related decline in motility observed in age-1 mutants with defects in the IIS pathway was also modulated by RME-1. The expression of sod-3, which is positively correlated with the remaining lifespan of an individual, was decreased by rme-1 knockdown. Our study demonstrates that RME-1 is required for the anti-aging effect associated with decreased IIS. We suggest that endocytic transport could be one underlying mechanisms for longevity via the IIS pathway.

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