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Cited by 169Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and Treatments

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

Turunc Bayrakdar, E., Uyanikgil, Y., Kanit, L., Koylu, E., Yalcin, A.·2014·Free Radical Research
DOI 10.3109/10715762.2013.857018
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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.

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Crossref · 10.3109/10715762.2013.857018

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Citations

Cites

Research works printed but not linked: 4

  1. Paglia DE, 1967, J Lab Clin Med, 70, 158
  2. Chomczynski P, 1993, Biotechniques, 15, 532
  3. Ferraris DV, 2010, From concept to clinic. J Med Chem, 53, 4561
  4. Behl C, 1997, J Neural Transm, 49, 125

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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
DOI
10.3109/10715762.2013.857018
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

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