ArticleMolecular neurobiology2024
COP-22 Alleviates D-Galactose-Induced Brain Aging by Attenuating Oxidative Stress, Inflammation, and Apoptosis in Mice.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Evaluation the role of quinoa seeds in attenuation the brain cellular senescence and aging induced by D-galactose and γ-radiation in rats: insights into autophagy, telomerase activity, amyloid-β and tau proteins.Inflammopharmacology · 2026Article
- Protocatechuic Acid Alleviates D-Gal-Induced Renal Senescence and Injury in Mice by Regulating Taurine Metabolism.Food science & nutrition · 2026Article
- RhFGF21 Mitigated D-gal-triggered Learning and Memory Dysfunction in Mice by Inhibiting Oxidative Stress, Inflammation and Senescence in Cortex and Hippocampus via Modulating FGFR1 and SIRT1.Molecular neurobiology · 2026Article
- Behavior and Musculoskeletal Effects of Chronic D-Galactose Treatment in Mice: Role of Heme Oxygenase-1.Biomolecules · 2026Article
- Periodic Therapeutic Phlebotomy Mitigates Systemic Aging Phenotypes by Promoting Bone Marrow Function.Aging cell · 2026Article
- Human adipose stem cell-derived exosomes modulate the transcriptome of D-galactose-Induced neuronal cells.Scientific reports · 2026Article
- Effects of herbal medicines and their phytoconstituents on vagus nerve stimulation: a systematic review ofFrontiers in pharmacology · 2026Review
- Mechanistic intersections of empagliflozin and nebivolol in aging-associated redox and inflammatory pathways.Frontiers in pharmacology · 2026Review
- The Potential of Ectoine as a Brain Anti-Aging Agent in Rat Model of D-Galactose-Accelerated Aging May Be Mediated Through Crosstalk Between Redox/Mitochondrial Homeostasis/Autophagic/Apoptotic Pathways.Molecular neurobiology · 2025Article
- miR-133b-3p Mitigates D-Galactose-Induced Hippocampal Neuron Aging Through Autophagy Regulation via the MAPK/ERK Signaling Pathway.Molecular neurobiology · 2025Article
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Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is a natural and inevitable process of organisms. With the intensification of population aging, research on aging has become a hot topic of global attention. The most obvious manifestation of human aging is the aging of brain function, which has been linked to the development of neurodegenerative diseases. In this study, COP-22, a mono-carbonyl curcumin derivative, was evaluated for its anti-aging ability, especially its ability to resist brain aging induced by D-galactose (D-gal) in mice. For brain protection, COP-22 could resist D-gal-induced oxidative stress by increasing the activity of antioxidative defense enzymes and enhancing antioxidant capacity in the brain tissue; COP-22 could improve the dysfunction of the cholinergic system by decreasing the increased activity of acetylcholinesterase and increasing the reduced content of acetylcholine induced by D-gal; and COP-22 could protect nerve cells of the brain. Further, western blot was used to determine related proteins of the brain. We found that COP-22 could effectively protect against brain injury (SIRT1, p53, p21, and p16) by inhibiting oxidative stress (Nrf2 and HO-1), inflammation (IL-6 and TNF-α), and apoptosis (Bax and caspase-3) in D-gal-induced aging mice. Additionally, COP-22 demonstrated the ability to reduce oxidative stress in serum and liver caused by D-gal, as well as relieve the damages in the liver and kidney induced by D-gal. These results indicated that COP-22 had potential anti-aging activity and could be used in the therapy of aging and aging-associated diseases like Alzheimer disease.
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