CoChat
Sign Up
Cited by 55Genetic Neurodegenerative DiseasesParkinson's Disease Mechanisms and TreatmentsMitochondrial Function and Pathology

Role of Rho Kinase Inhibition in the Protective Effect of Fasudil and Simvastatin Against 3-Nitropropionic Acid-Induced Striatal Neurodegeneration and Mitochondrial Dysfunction in Rats

Ahmed, Lamiaa A., Darwish, Hebatallah A., Abdelsalam, Rania M., Amin, HebatAllah A.·2016·Molecular Neurobiology
DOI 10.1007/s12035-015-9303-2
Open this paper in CoChat — free account

Abstract

3-Nitropropionic acid (3-NP)-induced neurotoxicity is an experimental model which mimics the pathology and motor abnormalities seen in Huntington's disease (HD) in human. The present investigation was directed to estimate the role of rho kinase (ROCK) inhibition in the possible protective effect of fasudil and simvastatin in 3-NP-induced striatal neurodegeneration in rats. Animals were injected s.c. with 3-NP (20 mg/kg/day) for 1 week with or without administration of fasudil (10 mg/kg/day, p.o.) or simvastatin (20 mg/kg/day, p.o.). At the end of experiment, motor and behavioral abnormalities were evaluated. Animals were then sacrificed for measurement of mitochondrial membrane potential as well as succinate dehydrogenase (SDH) and caspase-3 activities in striatum. Moreover, tumor necrosis factor-alpha (TNF-α) level and protein expressions of proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), ROCK, phosphorylated-Akt (p-Akt), endothelial and inducible nitric oxide synthase (eNOS and iNOS), Bax, and Bcl-2 were estimated. Finally, histological changes as demonstrated by striatum injury score, glial activation, and percentage of altered mitochondria were assessed. Both fasudil and simvastatin effectively inhibited 3-NP-induced behavioral, biochemical, and histological changes through inhibition of ROCK activity. However, fasudil provided more amelioration in histological changes, mitochondrial membrane potential and SDH activity in addition to p-Akt and PGC-1α p…

Integrity signals

Registry

Crossref · 10.1007/s12035-015-9303-2

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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 3-nitropropionic acid HD rat model, inhibition of RhoA/ROCK signaling using Fasudil or simvastatin inhibits 3-NP-induced neurotoxicity and mitochondrial dysfunction through a mechanism involving the ROCK/p-Akt/eNOS pathway.

    “In the 3-nitropropionic acid (3-NP) HD rat model, inhibition of RhoA/ROCK signaling using Fasudil or simvastatin inhibited 3-NP-induced neurotoxicity and, interestingly, also mitochondrial dysfunction through a mechanism involving the ROCK/p-Akt/eNOS pathway [206].”

    From RhoA Signaling in Neurodegenerative Diseases (2022) · cites this paper as [206]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Ahmed, L. A., Darwish, H. A., Abdelsalam, R. M., & Amin, H. A.
Affiliations
Cairo University (EG)
Corresponding author
Ahmed, Lamiaa A.
ORCID
Venue
Molecular Neurobiology
Publisher
Springer Science and Business Media LLC
Published
2015-07-15
Volume
53
Issue
6
Pages
3927-3938
ISSN
  • 0893-7648 (ISSN-L)
  • 1559-1182
DOI
10.1007/s12035-015-9303-2
OpenAlex
W1163715347
Cited by
55
References
2
Citations by year
2026: 4 · 2025: 6 · 2024: 8 · 2023: 6 · 2022: 9 · 2021: 6 · 2020: 7 · 2019: 6 · 2018: 3
FWCI
0.42
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Molecular Neurobiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
Rho kinase inhibition, fasudil, simvastatin, 3-nitropropionic acid, Huntington's disease, striatal degeneration, mitochondrial dysfunction, mitochondrial membrane potential, succinate dehydrogenase, caspase-3, PGC-1α, Akt signaling, endothelial nitric oxide synthase, inducible nitric oxide synthase, neuroprotection, neurotoxicity
MeSH terms
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Animals, Behavior, Animal, Body Weight, Corpus Striatum, Male, Mitochondria, Motor Activity, Nerve Degeneration, Nitro Compounds, Organ Size, Phosphorylation, Propionates, Succinate Dehydrogenase, Tumor Necrosis Factor-alpha, Rats, Wistar, Neuroprotective Agents, 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine, Simvastatin, Protein Kinase Inhibitors, bcl-2-Associated X Protein, Proto-Oncogene Proteins c-akt, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type III, Membrane Potential, Mitochondrial, Caspase 3, rho-Associated Kinases

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