The DOI matches its Crossref record; 94 of the 95 references it cites were found in a registry or an index.
Nicotinamide treatment reduces the levels of oxidative stress, apoptosis, and PARP-1 activity in Aβ(1–42)-induced rat model of Alzheimer's disease
Abstract
The underlying mechanisms of Alzheimer's Disease (AD) are still unclear. It is suggested that poly(ADP-ribose) polymerase-1 (PARP-1) overactivation can cause neuroinflammation and cell death. In this study we searched the effects of nicotinamide (NA), endogenous PARP-1 inhibitor, on oxidative stress, apoptosis, and the regulation of PARP-1 and nuclear factor kappa B (NF-κB) in amyloid beta peptide (1-42) (Aβ(1-42))-induced neurodegeneration. Sprague-Dawley rats were divided into four groups as control, Aβ(1-42), Aβ(1-42) + NA(100 and 500 mg/kg). All groups were stereotaxically injected bilaterally into the hippocampus with Aβ(1-42) or saline. After surgery NA administrations were made intraperitoneally (ip) for 7 days. In order to investigate the effects of Aβ(1-42) and NA, protein carbonyls, lipid peroxidation, reactive oxygen species (ROS) production, glutathione (GSH) levels, activities of antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase), mitochondrial function, mRNA and protein levels of PARP-1, NF-κB, p53, Bax, and Bcl-2 were measured in specific brain regions such as cortex and hippocampus. Aβ(1-42) treatment only increased the oxidative stress parameters and caused decline in antioxidant enzyme activities, mitochondrial function, and GSH levels. Also, overexpression of PARP-1, NF-κB, p53, Bax, and the decreased levels of Bcl-2 were observed in Aβ(1-42)-treated group. NA treatments against Aβ(1-42)-upregulated Bcl-2 and downregulated PARP-1, NF-κB, p53, and Bax levels. NA treatments also decreased the oxidative stress parameters and elevated antioxidant enzyme activities, GSH levels, and mitochondrial function against Aβ(1-42) treatment. These data suggest that NA may have a therapeutic potential in neurodegenerative processes due to the decreased levels of oxidative stress, apoptosis, and PARP-1 activity.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“In vivo studies using various Alzheimer disease and Parkinson disease models have shown that loss of PARP1 protects from brain dysfunctions and cognitive decline170–174.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [171]
In the citing paper
“PARP1 activation is also associated with Alzheimer disease170,171 and Parkinson disease172,173 pathogenesis.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [171]
Citations
Cites
PROTEIN MEASUREMENT WITH THE FOLIN PHENOL REAGENT
Lowry, O. H., Rosebrough, N., Farr, A. L., & Randall, R. (1951) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(19)52451-6 · Cited by 316,394
Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method
Livak, K. J., & Schmittgen, T. D. (2001) · Methods · doi:10.1006/meth.2001.1262 · Cited by 180,860
The rat brain in stereotaxic coordinates
Palkovits, M. (1983) · Neuropeptides · doi:10.1016/0143-4179(83)90049-5 · Cited by 28,959
The Rat Brain in Stereotaxic Coordinates
Paxinos, G., & Watson, C. (1983) · Elsevier eBooks · doi:10.1016/c2009-0-63235-9 · Cited by 28,585
Ellman, G. L. (1959) · Archives of Biochemistry and Biophysics · doi:10.1016/0003-9861(59)90090-6 · Cited by 26,824
Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase.
Paglia, D. E., & Valentine, W. N. (1967) · PubMed · Cited by 10,776
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607
[43] Malondialdehyde determination as index of lipid Peroxidation
Draper, H. H., & Hadley, M. (1990) · Methods in enzymology on CD-ROM/Methods in enzymology · doi:10.1016/0076-6879(90)86135-i · Cited by 4,291
Bustin, S. A. (2000) · Journal of Molecular Endocrinology · doi:10.1677/jme.0.0250169 · Cited by 3,844
Oxidative DNA damage: mechanisms, mutation, and disease
Cooke, M. S., Evans, M. D., Dizdaroglu, M., & Lunec, J. (2003) · The FASEB Journal · doi:10.1096/fj.02-0752rev · Cited by 3,245
Research works printed but not linked: 4
- Paglia DE, 1967, J Lab Clin Med, 70, 158
- Chomczynski P, 1993, Biotechniques, 15, 532
- Ferraris DV, 2010, From concept to clinic. J Med Chem, 53, 4561
- Behl C, 1997, J Neural Transm, 49, 125
Cited by
Sorted by citations
Cantó, C., Menzies, K. J., & Auwerx, J. (2015) · Cell Metabolism · doi:10.1016/j.cmet.2015.05.023 · Cited by 1,648
NAD+ metabolism and its roles in cellular processes during ageing
Covarrubias, A. J., Perrone, R., Grozio, A., & Verdin, E. (2021) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-00313-x · Cited by 1,617
Mitophagy and Alzheimer’s Disease: Cellular and Molecular Mechanisms
Kerr, J. S., Adriaanse, B. A., Greig, N. H., Mattson, M. P., Cader, M. Z., Bohr, V. A., & Fang, E. F. (2017) · Trends in Neurosciences · doi:10.1016/j.tins.2017.01.002 · Cited by 870
NAD+ homeostasis in health and disease
Katsyuba, E., Romani, M., Hofer, D., & Auwerx, J. (2020) · Nature Metabolism · doi:10.1038/s42255-019-0161-5 · Cited by 627
Lou, G., Palikaras, K., Lautrup, S., Scheibye‐Knudsen, M., Tavernarakis, N., & Fang, E. F. (2019) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2019.07.002 · Cited by 455
Metadata
- Authors
- Turunc Bayrakdar, E., Uyanikgil, Y., Kanit, L., Koylu, E., & Yalcin, A.
- Affiliations
- Ege University (TR)
- ORCID
- Koylu, E.
- Venue
- Free Radical Research
- Publisher
- Informa UK Limited
- Published
- 2013-11-11
- Volume
- 48
- Issue
- 2
- Pages
- 146-158
- ISSN
- 1029-2470 (ISSN-L)
- 1071-5762
- OpenAlex
- W1980204153
- Cited by
- 169
- References
- 95
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 16 · 2023: 13 · 2022: 13 · 2021: 17 · 2020: 17 · 2019: 17 · 2018: 13 · 2017: 15 · 2016: 8 · 2015: 17 · 2014: 11
- FWCI
- 8.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Free Radical Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- nicotinamide, Alzheimer's disease, amyloid-beta 42, oxidative stress, apoptosis, PARP1, NF-κB, p53, Bax, Bcl-2, neuroinflammation, neurodegeneration, hippocampus, antioxidant enzymes, glutathione, mitochondrial function, reactive oxygen species, lipid peroxidation
- MeSH terms
- Poly(ADP-ribose) Polymerase Inhibitors, Poly (ADP-Ribose) Polymerase-1, Alzheimer Disease, Animals, Antioxidants, Catalase, Drug Evaluation, Preclinical, Glutathione, Glutathione Peroxidase, Hippocampus, Humans, Male, Malondialdehyde, Niacinamide, Peptide Fragments, Poly(ADP-ribose) Polymerases, Superoxide Dismutase, Synaptosomes, Lipid Peroxidation, Gene Expression, Amyloid beta-Peptides, NF-kappa B, Rats, Sprague-Dawley, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Neuroprotective Agents, Apoptosis Regulatory Proteins, Rats
About these checks
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 ›
Are you an author, or do you see a problem with this page? Request a review
