T1-11, an adenosine derivative, ameliorates aging-related behavioral physiology and senescence markers in aging mice

Hsu, Wei-Hsiang; Shiao, Young‐Ji; Chao, Yen-Ming; Huang, Yun-Chen; Lin, Yun-Lian

doi:10.18632/aging.103279

Cited by 13 publications

(3 citation statements)

References 46 publications

(76 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To determine whether GA‐D can exert an anti‐aging effect in vivo, an aging mouse model was subjected to oxidative stress using d ‐gal (Hsu et al, 2020 ) (Figure 5a ). Firstly, the physical strength of mice in each group was measured via the weight‐loaded forced swimming test (Sun et al, 2020 ).…”

Section: Resultsmentioning

confidence: 99%

Ganoderic acid D prevents oxidative stress‐induced senescence by targeting 14‐3‐3ε to activate CaM/CaMKII/NRF2 signaling pathway in mesenchymal stem cells

Yuan

Luo

et al. 2022

Aging Cell

View full text Add to dashboard Cite

show abstract

Section: Resultsmentioning

confidence: 99%

Ganoderic acid D prevents oxidative stress‐induced senescence by targeting 14‐3‐3ε to activate CaM/CaMKII/NRF2 signaling pathway in mesenchymal stem cells

Yuan

Luo

et al. 2022

Aging Cell

View full text Add to dashboard Cite

show abstract

“…Furthermore, clinical studies have demonstrated the association between metabolic dysfunctions, neuroinflammation, and cognitive decline. For instance, a study by Hsu et al found that elevated markers of neuroinflammation, such as cytokines and chemokines, were associated with lower cognitive performance in individuals with metabolic syndrome [28].…”

Section: Introductionmentioning

confidence: 99%

Impact of NLRP3 Depletion on Aging-Related Metaflammation, Cognitive Function, and Social Behavior in Mice

Khilazheva,

Mosiagina,

Panina

et al. 2023

IJMS

View full text Add to dashboard Cite

Immunosenescence and chronic inflammation associated with old age accompany brain aging and the loss of complex behaviors. Neuroinflammation in the hippocampus plays a pivotal role in the development of cognitive impairment and anxiety. However, the underlying mechanisms have not been fully explained. In this study, we aimed to investigate the disruption of insulin signaling and the mechanisms underlying metabolic inflammation (“metaflammation”) in the brains of wild-type (WT) and NLRP3 knockout (KO) mice of different ages. We found a significant upregulation of the NLRP3 inflammasome in the hippocampus during aging, leading to an increase in the expression of phosphorylated metaflammation proteinases and inflammatory markers, along with an increase in the number of senescent cells. Additionally, metaflammation causes anxiety and impairs social preference behavior in aged mice. On the other hand, deletion of NLRP3 improves some behavioral and biochemical characteristics associated with aging, such as signal memory, neuroinflammation, and metabolic inflammation, but not anxious behavior. These results are associated with reduced IL-18 signaling and the PKR/IKKβ/IRS1 pathway as well as the SASP phenotype. In NLRP3 gene deletion conditions, PKR is down-regulated. Therefore, it is likely that slowing aging through various NLRP3 inhibition mechanisms will lessen the corresponding cognitive decline with aging. Thus, the genetic knockout of the NLRP3 inflammasome can be seen as a new therapeutic strategy for slowing down central nervous system (CNS) aging.

show abstract

“…Ali et al found that ovariectomized rats helps to preserve bone mass and biomechanical properties by feeding GlcN [ 12 ]. Kalbe et al reported that GlcN accelerates the early repair of tibial fractures in rats by increasing the activity of osteoblasts and promoting new bone formation [ 13 ]. Therefore, it is interesting to explore whether GlcN has a therapeutic effect on senile osteoporosis which caused by reduced osteogenesis.…”

Section: Introductionmentioning

confidence: 99%

Glucosamine delays the progression of osteoporosis in senile mice by promoting osteoblast autophagy

Huang

Zheng

et al. 2022

Nutr Metab (Lond)

View full text Add to dashboard Cite

Background Senile osteoporosis (SOP) is one of the most prevalent diseases that afflict the elderly population, which characterized by decreased osteogenic ability. Glucosamine (GlcN) is an over-the-counter dietary supplement. Our previous study reported that GlcN promotes osteoblast proliferation by activating autophagy in vitro. The purpose of this study is to determine the effects and mechanisms of GlcN on senile osteoporosis and osteogenic differentiation in vivo. Methods Aging was induced by subcutaneous injection of d-Galactose (d-Gal), and treated with GlcN or vehicle. The anti-senile-osteoporosis effect of GlcN was explored by examining changes in micro-CT, serum indicators, body weight, protein and gene expression of aging and apoptosis. Additionally, the effects of GlcN on protein and gene expression of osteogenesis and autophagy were observed by inhibiting autophagy with 3-methyladenine (3-MA). Results GlcN significantly improved bone mineral density (BMD) and bone micro-architecture, decreased skeletal senescence and apoptosis and increased osteogenesis in d-Gal induced osteoporotic mice. While all effect was reversed with 3-MA. Conclusion GlcN effectively delayed the progression of osteoporosis in senile osteoporotic mice by promoting osteoblast autophagy. This study suggested that GlcN may be a prospective candidate drug for the treatment of SOP.

show abstract

T1-11, an adenosine derivative, ameliorates aging-related behavioral physiology and senescence markers in aging mice

Cited by 13 publications

References 46 publications

Ganoderic acid D prevents oxidative stress‐induced senescence by targeting 14‐3‐3ε to activate CaM/CaMKII/NRF2 signaling pathway in mesenchymal stem cells

Ganoderic acid D prevents oxidative stress‐induced senescence by targeting 14‐3‐3ε to activate CaM/CaMKII/NRF2 signaling pathway in mesenchymal stem cells

Impact of NLRP3 Depletion on Aging-Related Metaflammation, Cognitive Function, and Social Behavior in Mice

Glucosamine delays the progression of osteoporosis in senile mice by promoting osteoblast autophagy

Contact Info

Product

Resources

About