Urolithin-A Derivative UAS03 Improves Cognitive Deficits and Memory by Activating Nrf2 Pathways to Alleviate Oxidative Stress and Neuroinflammation DOI

Dipan Maity,

Vikrant Rahi,

Sandya Tambi Dorai

et al.

ACS Chemical Neuroscience, Journal Year: 2025, Volume and Issue: unknown

Published: April 14, 2025

Neuroinflammation is a key factor in age-related cognitive decline and memory impairment. UAS03, potent synthetic analogue of Urolithin-A, has demonstrated anti-inflammatory antioxidant properties. This investigation examined the neuroprotective effect UAS03 on lipopolysaccharide (LPS) induced neuroinflammation, its associated impairments, deficits, depression-like behaviors. Intracerebroventricular administration LPS (12 μg/kg) was performed to induce neuroinflammation mice, followed by 7 day treatment with at 10 30 mg/kg doses. Mice were evaluated for depressive anxiety-like behavior, spatial memory, learning functions using series neurobehavioral test paradigms. Histopathological molecular analyses conducted hematoxylin-eosin cresyl violet staining, immunohistochemistry, ELISA, Western blotting techniques. We have found that, significantly enhanced impaired while concurrently reducing symptoms. Furthermore, compound attenuated neuronal damage decreased expression IBA-1 GFAP hippocampal region. Through activation nuclear erythroid 2-related 2 (Nrf2) signaling pathway, effectively mitigated markers oxidative stress reduced levels pro-inflammatory factors, including IL-1β, TNF-α, COX-2. Cumulatively, this study provides compelling evidence that exerts effects regulating essential pathways involved mechanisms, suggesting potential as preventative measure against impairments neuroinflammation.

Language: Английский

Global research trends in inflammaging from 2005 to 2024: a bibliometric analysis DOI Creative Commons
Beier Jiang, Y.C. Dong, Yu Xiong

et al.

Frontiers in Aging, Journal Year: 2025, Volume and Issue: 6

Published: April 10, 2025

Inflammaging, defined as chronic low-grade inflammation associated with aging, is considered a key factor in many age-related diseases. Despite growing research, comprehensive assessments of trends and focuses on this field over the past 2 decades remain lacking. To comprehensively analyze literature development trends, scientific priorities, their evolution inflammaging from 2005 to 2024 using bibliometric analysis. Academic was retrieved Web Science Core Collection. CiteSpace software used tool annual publication contributing countries/regions, leading research institutions, primary journals, keyword co-occurrence, including clustering burst analysis field. The study included 1,800 eligible articles, demonstrating consistent growth publications 20 years. United States Italy were principal contributors. University Bologna had highest publication. Professor Claudio Franceschi has been figure Journal shows that themes predominantly focus molecular biology/immunology medicine/clinical fields. Keyword identifies major hotspots "inflammaging," "Crohn's disease," "periodontitis," "immunosenescence," "skeletal muscle," "gut microbiota," "Parkinson's disease." Emerging term indicates shift specific inflammatory diseases broader aging immune modulation studies. This first systematic assessment reveals sustained academic an increasingly deep focus.

Language: Английский

Citations

0
Urolithin-A Derivative UAS03 Improves Cognitive Deficits and Memory by Activating Nrf2 Pathways to Alleviate Oxidative Stress and Neuroinflammation DOI

Dipan Maity,

Vikrant Rahi,

Sandya Tambi Dorai

et al.

ACS Chemical Neuroscience, Journal Year: 2025, Volume and Issue: unknown

Published: April 14, 2025

Neuroinflammation is a key factor in age-related cognitive decline and memory impairment. UAS03, potent synthetic analogue of Urolithin-A, has demonstrated anti-inflammatory antioxidant properties. This investigation examined the neuroprotective effect UAS03 on lipopolysaccharide (LPS) induced neuroinflammation, its associated impairments, deficits, depression-like behaviors. Intracerebroventricular administration LPS (12 μg/kg) was performed to induce neuroinflammation mice, followed by 7 day treatment with at 10 30 mg/kg doses. Mice were evaluated for depressive anxiety-like behavior, spatial memory, learning functions using series neurobehavioral test paradigms. Histopathological molecular analyses conducted hematoxylin-eosin cresyl violet staining, immunohistochemistry, ELISA, Western blotting techniques. We have found that, significantly enhanced impaired while concurrently reducing symptoms. Furthermore, compound attenuated neuronal damage decreased expression IBA-1 GFAP hippocampal region. Through activation nuclear erythroid 2-related 2 (Nrf2) signaling pathway, effectively mitigated markers oxidative stress reduced levels pro-inflammatory factors, including IL-1β, TNF-α, COX-2. Cumulatively, this study provides compelling evidence that exerts effects regulating essential pathways involved mechanisms, suggesting potential as preventative measure against impairments neuroinflammation.

Language: Английский

Citations

0