scholarly journals Effects of Lycium barbarum Polysaccharides on Health and Aging of C. elegans Depend on daf-12/daf-16

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Zhaokang Zhang ◽  
Yannan Zhou ◽  
Haitao Fan ◽  
Kirunda John Billy ◽  
Yunjie Zhao ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Aging Process ◽  
Functional Foods ◽  
Mrna Expression Level ◽  
Lycium Barbarum ◽  
C Elegans ◽  
Age Related ◽  
Aging And Health ◽  
Global Population ◽  
Lycium Barbarum Polysaccharides

As the global population ages, searching for drugs and functional foods which can slow down the aging process has attracted a number of researchers. In this paper, the Lycium barbarum polysaccharides (LBP) extracted from Lycium barbarum was characterized and the effects of LBP on the aging and health of C. elegans were studied. Results showed that LBP can prolong the lifespan, improve the abilities to withstand environmental stress, enhance reproductive potentials, and maintain muscle integrity of C. elegans. By using genetically mutated C. elegans strains, RNAi gene silencing, and measuring the mRNA expression level, it was demonstrated that the lifespan of C. elegans was extended by LBP mainly through sir-2.1, daf-12, and daf-16. The present study might provide a basis for further study of LBP as a food or drug to interfere with aging and reduce the incidence of age-related diseases.

scholarly journals Phenotypic Screening in C. elegans as a Tool for the Discovery of New Geroprotective Drugs

2020 ◽  
Vol 13 (8) ◽  
pp. 164 ◽  
Author(s):  
Sven Bulterijs ◽  
Bart P. Braeckman
Keyword(s):  
High Throughput ◽  
High Throughput Screening ◽  
Aging Process ◽  
Population Aging ◽  
Model Organisms ◽  
Pharmacological Interventions ◽  
C Elegans ◽  
System A ◽  
Age Related ◽  
Screening Strategies

Population aging is one of the largest challenges of the 21st century. As more people live to advanced ages, the prevalence of age-related diseases and disabilities will increase placing an ever larger burden on our healthcare system. A potential solution to this conundrum is to develop treatments that prevent, delay or reduce the severity of age-related diseases by decreasing the rate of the aging process. This ambition has been accomplished in model organisms through dietary, genetic and pharmacological interventions. The pharmacological approaches hold the greatest opportunity for successful translation to the clinic. The discovery of such pharmacological interventions in aging requires high-throughput screening strategies. However, the majority of screens performed for geroprotective drugs in C. elegans so far are rather low throughput. Therefore, the development of high-throughput screening strategies is of utmost importance.

scholarly journals The Effect of Lycium barbarum Polysaccharides on Pyroptosis-Associated Amyloid β1-40 Oligomers-Induced Adult Retinal Pigment Epithelium 19 Cell Damage

2020 ◽  
Vol 21 (13) ◽  
pp. 4658 ◽  
Author(s):  
Ming Yang ◽  
Kwok-Fai So ◽  
Amy Cheuk Yin Lo ◽  
Wai Ching Lam
Keyword(s):  
Retinal Pigment Epithelium ◽  
Cell Viability ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Morphological Characteristics ◽  
Age Related Macular Degeneration ◽  
Dependent Manner ◽  
Lycium Barbarum ◽  
Age Related ◽  
Lycium Barbarum Polysaccharides

Age-related macular degeneration (AMD) is a sight-threatening disease with limited treatment options. We investigated whether amyloid β1-40 (Aβ1-40) could cause pyroptosis and evaluated the effects of Lycium barbarum polysaccharides (LBP) on Aβ1-40 oligomers-induced retinal pigment epithelium 19 (ARPE-19) damage, which is an in vitro AMD model. Aβ1-40 oligomers verified by Western blot were added to ARPE-19 cells with or without 24 h LBP treatment. Aβ1-40 oligomers significantly decreased ARPE-19 cell viability with obvious morphological changes under light microscopy. SEM revealed swollen cells with a bubbling appearance and ruptured cell membrane, which are morphological characteristics of pyroptosis. ELISA results showed increased expression of IL-1β and IL-18, which are the final products of pyroptosis. LBP administration for 24 h had no toxic effects on ARPE-19 cells and improved cell viability and morphology while disrupting Aβ1-40 oligomerization in a dose-dependent manner. Furthermore, Aβ1-40 oligomers up-regulated the cellular immunoreactivity of pyroptosis markers including NOD-like receptors protein 3 (NLRP3), caspase-1, and membrane N-terminal cleavage product of GSDMD (GSDMD-N), which could be reversed by LBP treatment. Taken together, this study showed that LBP effectively protects the Aβ1-40 oligomers-induced pyroptotic ARPE-19 cell damages by its anti-Aβ1-40 oligomerization properties and its anti-pyroptotic effects.

A Pro-Somathropic Formulation with GHR Agonistic and Pro-Thyrogenic Features (Preprint)

2019 ◽  
Author(s):  
Erdal Can Alkoclar
Keyword(s):  
Mrna Expression ◽  
Efficient Method ◽  
Age Related

BACKGROUND A Formulation consisting of 2 Dioscin and 2 Glucopyranoside Derivatives with Simultaneous GHRH Stimulative and T3 mRNA Expression Enhancimg Features. OBJECTIVE Anti Aging METHODS GH/T3 Optimization RESULTS Approved in Vitro CONCLUSIONS Endogenous GH and T3 Optimization is the an efficient method for combating age related Senility and Fatigue Symptoms

scholarly journals Two human metabolites rescue a C. elegans model of Alzheimer’s disease via a cytosolic unfolded protein response

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Priyanka Joshi ◽  
Michele Perni ◽  
Ryan Limbocker ◽  
Benedetta Mannini ◽  
Sam Casford ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Unfolded Protein Response ◽  
Neurodegenerative Disorders ◽  
C Elegans ◽  
Unfolded Protein ◽  
Model Of Alzheimer’S Disease ◽  
Age Related ◽  
Parkinson’S Diseases ◽  
Protein Response

AbstractAge-related changes in cellular metabolism can affect brain homeostasis, creating conditions that are permissive to the onset and progression of neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases. Although the roles of metabolites have been extensively studied with regard to cellular signaling pathways, their effects on protein aggregation remain relatively unexplored. By computationally analysing the Human Metabolome Database, we identified two endogenous metabolites, carnosine and kynurenic acid, that inhibit the aggregation of the amyloid beta peptide (Aβ) and rescue a C. elegans model of Alzheimer’s disease. We found that these metabolites act by triggering a cytosolic unfolded protein response through the transcription factor HSF-1 and downstream chaperones HSP40/J-proteins DNJ-12 and DNJ-19. These results help rationalise previous observations regarding the possible anti-ageing benefits of these metabolites by providing a mechanism for their action. Taken together, our findings provide a link between metabolite homeostasis and protein homeostasis, which could inspire preventative interventions against neurodegenerative disorders.

scholarly journals Crosstalk between Different DNA Repair Pathways Contributes to Neurodegenerative Diseases

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 163
Author(s):  
Swapnil Gupta ◽  
Panpan You ◽  
Tanima SenGupta ◽  
Hilde Nilsen ◽  
Kulbhushan Sharma
Keyword(s):  
Dna Repair ◽  
Neurodegenerative Diseases ◽  
3D Models ◽  
Model Systems ◽  
Spinocerebellar Ataxias ◽  
C Elegans ◽  
Cellular Processes ◽  
Age Related ◽  
Damage Response ◽  
Lateral Sclerosis

Genomic integrity is maintained by DNA repair and the DNA damage response (DDR). Defects in certain DNA repair genes give rise to many rare progressive neurodegenerative diseases (NDDs), such as ocular motor ataxia, Huntington disease (HD), and spinocerebellar ataxias (SCA). Dysregulation or dysfunction of DDR is also proposed to contribute to more common NDDs, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), and Amyotrophic Lateral Sclerosis (ALS). Here, we present mechanisms that link DDR with neurodegeneration in rare NDDs caused by defects in the DDR and discuss the relevance for more common age-related neurodegenerative diseases. Moreover, we highlight recent insight into the crosstalk between the DDR and other cellular processes known to be disturbed during NDDs. We compare the strengths and limitations of established model systems to model human NDDs, ranging from C. elegans and mouse models towards advanced stem cell-based 3D models.

scholarly journals Steroid hormones sulfatase inactivation extends lifespan and ameliorates age-related diseases

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Mercedes M. Pérez-Jiménez ◽  
José M. Monje-Moreno ◽  
Ana María Brokate-Llanos ◽  
Mónica Venegas-Calerón ◽  
Alicia Sánchez-García ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Caenorhabditis Elegans ◽  
Protein Aggregation ◽  
Steroid Hormones ◽  
Sensory Neurons ◽  
Environmental Cues ◽  
Steroid Sulfatase ◽  
Loss Of Function ◽  
C Elegans ◽  
Age Related

AbstractAging and fertility are two interconnected processes. From invertebrates to mammals, absence of the germline increases longevity. Here we show that loss of function of sul-2, the Caenorhabditis elegans steroid sulfatase (STS), raises the pool of sulfated steroid hormones, increases longevity and ameliorates protein aggregation diseases. This increased longevity requires factors involved in germline-mediated longevity (daf-16, daf-12, kri-1, tcer-1 and daf-36 genes) although sul-2 mutations do not affect fertility. Interestingly, sul-2 is only expressed in sensory neurons, suggesting a regulation of sulfated hormones state by environmental cues. Treatment with the specific STS inhibitor STX64, as well as with testosterone-derived sulfated hormones reproduces the longevity phenotype of sul-2 mutants. Remarkably, those treatments ameliorate protein aggregation diseases in C. elegans, and STX64 also Alzheimer’s disease in a mammalian model. These results open the possibility of reallocating steroid sulfatase inhibitors or derivates for the treatment of aging and aging related diseases.

scholarly journals Natural variation in fecundity is correlated with species-wide levels of divergence in Caenorhabditis elegans

2021 ◽  
Author(s):  
Gaotian Zhang ◽  
Jake D Mostad ◽  
Erik C Andersen
Keyword(s):  
Life History ◽  
Caenorhabditis Elegans ◽  
Life History Traits ◽  
Life History Trait ◽  
Selective Sweeps ◽  
C Elegans ◽  
Genome Wide ◽  
Genetic Complexity ◽  
Genomic Regions ◽  
Global Population

Abstract Life history traits underlie the fitness of organisms and are under strong natural selection. A new mutation that positively impacts a life history trait will likely increase in frequency and become fixed in a population (e.g. a selective sweep). The identification of the beneficial alleles that underlie selective sweeps provides insights into the mechanisms that occurred during the evolution of a species. In the global population of Caenorhabditis elegans, we previously identified selective sweeps that have drastically reduced chromosomal-scale genetic diversity in the species. Here, we measured the fecundity of 121 wild C. elegans strains, including many recently isolated divergent strains from the Hawaiian islands and found that strains with larger swept genomic regions have significantly higher fecundity than strains without evidence of the recent selective sweeps. We used genome-wide association (GWA) mapping to identify three quantitative trait loci (QTL) underlying the fecundity variation. Additionally, we mapped previous fecundity data from wild C. elegans strains and C. elegans recombinant inbred advanced intercross lines that were grown in various conditions and detected eight QTL using GWA and linkage mappings. These QTL show the genetic complexity of fecundity across this species. Moreover, the haplotype structure in each GWA QTL region revealed correlations with recent selective sweeps in the C. elegans population. North American and European strains had significantly higher fecundity than most strains from Hawaii, a hypothesized origin of the C. elegans species, suggesting that beneficial alleles that caused increased fecundity could underlie the selective sweeps during the worldwide expansion of C. elegans.

Sign in / Sign up

Export Citation Format

Share Document