ArticleEvidence-based complementary and alternative medicine : eCAM2011
KIOM-4 Protects against Oxidative Stress-Induced Mitochondrial Damage in Pancreatic β-cells via Its Antioxidant Effects.
Article in Evidence-based complementary and alternative medicine : eCAM, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Pyrroloquinoline quinone alleviates oxidative damage induced by high glucose in HepG2 cells.Saudi journal of biological sciences · 2021Article
- Effectiveness of Magnolol, a Lignan from Magnolia Bark, in Diabetes, Its Complications and Comorbidities-A Review.International journal of molecular sciences · 2021Review
- Treatment With Naringenin Elevates the Activity of Transcription Factor Nrf2 to Protect Pancreatic β-Cells From Streptozotocin-Induced DiabetesFrontiers in pharmacology · 2018Article
- Elucidation of Molecular Mechanisms of Streptozotocin-Induced Oxidative Stress, Apoptosis, and Mitochondrial Dysfunction in Rin-5F PancreaticOxidative medicine and cellular longevity · 2017Article
- Nanoceria Attenuated High Glucose-Induced Oxidative Damage in HepG2 Cells.Cell journal · 2016Article
- Mulberry fruit extract protects pancreatic β-cells against hydrogen peroxide-induced apoptosis via antioxidative activity.Molecules (Basel, Switzerland) · 2014Article
- Therapeutic potential of pterostilbene against pancreatic beta-cell apoptosis mediated through Nrf2.British journal of pharmacology · 2014Article
- Protective Mechanism of KIOM-4 in Streptozotocin-Induced Pancreatic β-Cells Damage Is Involved in the Inhibition of Endoplasmic Reticulum Stress.Evidence-based complementary and alternative medicine : eCAM · 2011Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protective effect of KIOM-4, a mixture of plant extracts, was examined against streptozotocin (STZ)-induced mitochondrial oxidative stress in rat pancreatic β-cells (RINm5F). KIOM-4 scavenged superoxide and hydroxyl radicals generated by xanthine/xanthine oxidase and Fenton reaction (FeSO(4)/H(2)O(2)), respectively, in a cell-free chemical system. In addition, a marked increase in mitochondrial reactive oxygen species (ROS) was observed in STZ-induced diabetic cells; this increase was attenuated by KIOM-4 treatment. Mitochondrial manganese superoxide dismutase (Mn SOD) activity and protein expression were down-regulated by STZ treatment and up-regulated by KIOM-4 treatment. In addition, NF-E2 related factor 2 (Nrf2), a transcription factor for Mn SOD, was up-regulated by KIOM-4. KIOM-4 prevented STZ-induced mitochondrial lipid peroxidation, protein carbonyl and DNA modification. Moreover, KIOM-4 treatment restored the loss of mitochondrial membrane potential (Δψ) that was induced by STZ treatment, and inhibited the translocation of cytochrome c from the mitochondria to the cytosol. In addition, KIOM-4 treatment elevated the level of ATP, succinate dehydrogenase activity and insulin level, which were reduced by STZ treatment. These results suggest that KIOM-4 exhibits a protective effect through its antioxidant effect and the attenuation of mitochondrial dysfunction in STZ-induced diabetic cells.
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Registered trials
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