RETRACTED: Natural Dietary Supplementation of Curcumin Protects Mice Brains against Ethanol-Induced Oxidative Stress-Mediated Neurodegeneration and Memory Impairment via Nrf2/TLR4/RAGE Signaling
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The aim of the current study was to explore the underlying neuroprotective mechanisms of curcumin (50 mg/kg, for six weeks) against ethanol (5 mg/kg i.p., for six weeks) induced oxidative stress and inflammation-mediated cognitive dysfunction in mice. According to our findings, ethanol triggered reactive oxygen species (ROS), apoptosis, neuroinflammation, and memory impairment, which were significantly inhibited with the administration of curcumin, as assessed by ROS, lipid peroxidation (LPO), and Nrf2/HO-1 (nuclear factor erythroid 2-related factor 2/Heme-oxygenase-1) expression in the experimental mice brains. Moreover, curcumin regulated the expression of the glial cell markers in ethanol-treated mice brains, as analyzed by the relative expression TLR4 (Toll like Receptor 4), RAGE (Receptor for Advanced Glycations End products), GFAP (Glial fibrillary acidic protein), and Iba-1 (Ionized calcium binding adaptor molecule 1), through Western blot and confocal microscopic analysis. Moreover, our results showed that curcumin downregulated the expression of p-JNK (Phospo c-Jun N-Terminal Kinase), p-NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells), and its downstream targets, as assessed by Western blot and confocal microscopic analysis. Finally, the expression of synaptic proteins and the behavioral results also supported the hypothesis that curcumin may inhibit memory dysfunction and behavioral alterations associated with ethanol intoxication. Altogether, to the best of our knowledge, we believe that curcumin may serve as a potential, promising, and cheaply available neuroprotective compound against ethanol-associated neurodegenerative diseases.
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The AGE-RAGE axis has a contributing role in alcohol-induced neuroinflammation and neurodegeneration through elevated oxidative stress and upregulated cell death pathways in the brain.
“These results strongly suggest a contributing role of the AGE-RAGE axis in alcohol-induced neuroinflammation and neurodegeneration through elevated oxidative stress and upregulated cell death pathways in the brain.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [202]
Chronic exposure to alcohol enhances RAGE expression, ROS generation, Nrf2, TLR-4, GFAP, Iba1, and lipid peroxidation, resulting in neuroinflammation, neuronal apoptosis, and memory impairment.
“Additionally, chronic exposure to alcohol enhances RAGE expression, ROS generation, nuclear factor erythroid 2–related factor 2 (Nrf2), TLR-4, glial fibrillary acidic protein (GFAP), ionized calcium-binding adapter molecule 1 (Iba1), and lipid peroxidation, resulting in neuroinflammation, neuronal apoptosis, and memory impairment202.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [202]
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Nutraceuticals: A strategy to mitigate neurotoxicity
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- Authors
- Ikram, M., Saeed, K., Khan, A., Muhammad, T., Khan, M., Jo, M., Rehman, S., & Kim, M.
- Affiliations
- Gyeongsang National University (KR)
- Corresponding author
- Kim, Myeong
- Venue
- Nutrients
- Publisher
- MDPI AG
- Published
- 2019-05-15
- Volume
- 11
- Issue
- 5
- Pages
- 1082
- ISSN
- 2072-6643 (ISSN-L)
- PMC
- PMC6566393
- OpenAlex
- W2946669825
- Cited by
- 97
- References
- 57
- Citations by year
- 2026: 8 · 2025: 5 · 2024: 13 · 2023: 8 · 2022: 12 · 2021: 18 · 2020: 26 · 2019: 7
- FWCI
- 5.42
- Type
- journal article
- Language
- en
- Status
- Retracted
- Update notices
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- Nutrients (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Curcumin's Biomedical Applications
- Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- curcumin, ethanol neurotoxicity, oxidative stress, neuroinflammation, memory impairment, Nrf2/HO-1 pathway, TLR4, RAGE, JNK, NF-kB, reactive oxygen species, lipid peroxidation, glial cell markers, synaptic proteins, neuroprotection, retracted article
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Cell Line, Curcumin, Gene Expression Regulation, Hippocampus, Male, Memory Disorders, Mice, Inbred C57BL, Neurons, Lipid Peroxidation, Reactive Oxygen Species, Microglia, Oxidative Stress, Dietary Supplements, Neurodegenerative Diseases, RNA Interference, RNA, Small Interfering, Toll-Like Receptor 4, NF-E2-Related Factor 2, Mice
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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