ArticleMolecular neurobiology2025
Caffeic Acid Attenuates Neuronal Apoptosis, Oxidative Stress, and Memory Deficits via Antioxidant Properties in Aging Rats Induced by D-Galactose.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Article
- Article
- Caffeic Acid Ameliorates l-Methionine-Induced Hyperhomocysteinemia, Leading to Decreased Adult Neurogenesis and Oxidative Stress Status in Adult Rats.ACS chemical neuroscience · 2026Article
- Caffeic Acid and Human Health: Evidence-Based Roles in Disease Prevention and Treatment.International journal of molecular sciences · 2026Review
- Osteoarthritis and dementia: contrasting disorders driven by mutual pathways of autophagy, mTOR, GLP-1, AMPK, Wnt, and WISP1.Expert review of clinical pharmacology · 2026Review
- Agitation, Alzheimer's disease, and autophagy: mechanistic insights into aging pathways, gut microbiome, and artificial intelligence.Frontiers in immunology · 2026Review
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
- Review
- The Antiaging Potential of Dietary Plant-Based Polyphenols: A Review on Their Role in Cellular Senescence Modulation.Nutrients · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Aging is a main factor related to cognitive deficits. D-Galactose (D-gal), a monosaccharide, increases oxidative stress leading to cellular senescence, memory deficits, and neuronal apoptosis. Caffeic acid (CA) is an antioxidant that can interrupt free radicals and reduce oxidative stress. The present study purposely evaluated the benefits of CA in attenuating loss of neuronal apoptosis, oxidative stress, and memory in D-gal-activated rat brain aging. Male Sprague-Dawley rats were arbitrarily allocated into 6 groups (9 rats per group). The D-gal group was intraperitoneal (i.p.) injected with D-gal (50 mg/kg). The CA groups were orally given 20 or 40 mg/kg CA for 8 weeks. During that time, the co-treatment groups were given 50 mg/kg of D-gal and 20 or 40 mg/kg of CA. The results reveal that animals receiving only D-gal showed memory deficit in both the novel object location (NOL) and novel object recognition (NOR) tests. Reduction in scavenging enzyme activities and levels of B-cell lymphoma 2 (Bcl-2) protein expression were detected in the D-gal group. Furthermore, D-gal treatment significantly enhanced in the number of p21 positive cells in the subgranular zone (SGZ) of the hippocampal dentate gyrus, Bcl-2 associated X protein (Bax) and caspase3 protein expression, and malondialdehyde (MDA) levels. By contrast, both 20 and 40 mg/kg CA treatment alleviated these effects. These consequences confirmed that D-gal-activated brain aging led to enhancing apoptotic protein expression including Bcl-2, Bax, and caspase3 and memory impairments. Nevertheless, CA attenuated these effects in brain aging induced by D-gal via antioxidant properties.
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Registered trials
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