Cited by 21Coenzyme Q10 studies and effectsPancreatic function and diabetesMitochondrial Function and Pathology

Coenzyme Q10 suppresses apoptosis of mouse pancreatic β-cell line MIN6

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Sumi, Keisuke, Okura, Tsuyoshi, Fujioka, Youhei, Kato, Masahiko, Imamura, Takeshi, Taniguchi, Shin-ichi, Yamamoto, Kazuhiro·2018·Diabetology & Metabolic Syndrome

Abstract

BACKGROUND: In mitochondrial diabetes, apoptosis of β-cells caused by mitochondrial stress plays an important role in impaired insulin secretion. Several studies have reported that coenzyme Q10 (CoQ10) has therapeutic effects on mitochondrial diabetes, but no reports have examined the fundamental effectiveness or mechanism of CoQ10 in mitochondrial diabetes. We previously reported in a Japanese article that CoQ10 has protective effects on pancreatic β-cells against mitochondrial stress using mouse pancreatic β-cell line MIN6 and staurosporine (STS). Here, we report that CoQ10 protects MIN6 cells against apoptosis caused by STS and describe the more detailed apoptotic cascade. METHODS: Apoptosis of MIN6 cells was induced by 0.5 µM STS treatment for specific periods with or without 30 μM CoQ10. The apoptosis cascade in MIN6 cells was then investigated using WST-8 assays, annexin-V staining, western blotting, and DNA degradation analysis. RESULTS: Sixteen hours of 0.5 μM STS treatment led to 47% cell viability, but pretreatment with 30 μM CoQ10 resulted in significantly higher viability of 76% (P < 0.01). CoQ10 also prevented translocation of phosphatidylserine from the inner leaflet to the outer leaflet of the cell membrane. CoQ10 prevented cytochrome c release from mitochondria and activation of caspase-3. CONCLUSION: We concluded that CoQ10 protects pancreatic β-cells through anti-apoptotic effects against STS treatment.

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  • CoQ10 inhibits activation of caspase-3 and release of cytochrome c from mitochondria by stabilizing the mitochondrial membrane, suppresses proapoptotic genes caspase-3 and Bax, stimulates antiapoptotic Bcl2, and prevents translocation of nuclear apoptosis-inducing factors.

    “This is in line with Sumi et al. (2018) and Fatima et al. (2021) who stated that CoQ10 inhibited the activation of caspase-3 and the release of cytochrome c from mitochondria via stabilizing the mitochondrial membrane, thus preventing the release of apoptotic mediators.”

    From Can coenzyme Q10 alleviate the toxic effect of fenofibrate on skeletal muscle? (2023) · cites this paper as Sumi et al. 2018

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References 11 · Cited by 21

Research works printed but not linked: 1

  1. [8]Sumi K Coenzyme Q10 suppresses the apoptosis of mouse pancreatic beta-cell line MIN6 J Yonago Med Assoc 2013 64 33 39 PMC6000937 29942356

Authors
Sumi, K., Okura, T., Fujioka, Y., Kato, M., Imamura, T., Taniguchi, S.-I., & Yamamoto, K.
Affiliations
Tottori University (JP)
Corresponding author
Okura, Tsuyoshi
Venue
Diabetology & Metabolic Syndrome
Published
2018-06-14
Volume
10
Issue
1
Pages
47-47
ISSN
1758-5996 (ISSN-L)
OpenAlex
W2807824702
Cited by
21
References
11
Citations by year
2026: 3 · 2025: 4 · 2023: 3 · 2022: 3 · 2021: 2 · 2020: 3 · 2019: 2 · 2018: 1
FWCI
0.71
Type
journal article
Language
en
Open access
Locations
  • Diabetology & Metabolic Syndrome (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, other-oa)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • Tottori University research result repository (Tottori University) (submittedVersion, cc-by)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
coenzyme Q10, apoptosis, pancreatic beta cells, MIN6 cells, mitochondrial diabetes, staurosporine, mitochondrial stress, cytochrome c release, caspase-3 activation, phosphatidylserine translocation, anti-apoptotic effects

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