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Cited by 41Coenzyme Q10 studies and effectsMitochondrial Function and PathologyNeurological Disorders and Treatments

Coenzyme Q10 protects SHSY5Y neuronal cells from beta amyloid toxicity and oxygen‐glucose deprivation by inhibiting the opening of the mitochondrial permeability transition pore

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Li, Geng, Zou, Liang‐Yu, Cao, Chun‐Mei, Yang, Edward S.·2005·BioFactors
DOI 10.1002/biof.5520250111
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Abstract

Coenzyme Q10 (CoQ10) is an essential biological cofactor which increases brain mitochondrial concentration and exerts neuroprotective effects. In the present study, we exposed SHSY5Y neuroblastoma cells to neurotoxic beta amyloid peptides (Aβ) and oxygen glucose deprivation (OGD) to investigate the neuroprotective effect of 10μM CoQ10 by measuring (i) cell viability by the MTT assay, (ii) opening of the mitochondrial permeability transition pore via the fluorescence intensity of calcein‐AM, and (iii) superoxide anion concentration by hydroethidine. Cell viability (mean ± S.E.M.) was 55.5 ± 0.8% in the group exposed to Aβ + OGD, a value lower than that in the Aβ or OGD group alone (P<0.01). CoQ10 had no neuroprotective effect on cell death induced by either Aβ or OGD, but increased cell survival in the Aβ + OGD group to 57.3 ± 1.7%, which was higher than in the group treated with vehicle (P<0.05). The neuroprotective effect of CoQ10 was blocked by administration of 20μM atractyloside. Pore opening and superoxide anion concentration were increased in the Aβ + OGD group relative to sham control (P<0.01), and were attenuated to the sham level (P>0.05) when CoQ10 was administered. Our results demonstrate that CoQ10 protects neuronal cells against Aβ neurotoxicity together with OGD by inhibiting the opening of the pore and reducing the concentration of superoxide anion.

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  • CoQ10 protects SHSY5Y neuronal cells from β-amyloid toxicity through inhibition of the MPT pore.

    “CoQ10 protects SHSY5Y neuronal cells from β-amyloid toxicity through inhibition of the MPT pore144.”

    From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [144]

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Authors
Li, G., Zou, L., Cao, C., & Yang, E. S.
Affiliations
University of Hong Kong (HK)
Corresponding author
Li, Geng
ORCID
Venue
BioFactors
Publisher
Wiley
Published
2005-01
Volume
25
Issue
1-4
Pages
97-107
ISSN
  • 0951-6433 (ISSN-L)
  • 1872-8081
DOI
10.1002/biof.5520250111
OpenAlex
W1989477951
Cited by
41
References
58
Citations by year
2025: 2 · 2024: 1 · 2023: 1 · 2021: 1 · 2020: 4 · 2018: 5 · 2017: 2 · 2016: 2 · 2015: 1 · 2014: 3 · 2013: 3 · 2012: 4
FWCI
0.38
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 1448 d)
Locations
  • BioFactors (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
Keywords
coenzyme Q10, amyloid-beta toxicity, oxygen-glucose deprivation, mitochondrial permeability transition pore, neuroprotection, SHSY5Y neuroblastoma cells, superoxide, atractyloside, neuronal cell death, mitochondrial dysfunction
MeSH terms
Mitochondrial Permeability Transition Pore, Atractyloside, Cell Survival, Coenzymes, Fluoresceins, Glucose, Humans, Neuroblastoma, Neurons, Superoxides, Ubiquinone, Cell Hypoxia, Amyloid beta-Peptides, Mitochondrial Membrane Transport Proteins, Lactate Dehydrogenases, Cell Line, Tumor

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