Evidence map›Paper›PMID 39449772›Full record

ArticleIranian journal of medical sciences2024

Evaluation of Antioxidant Effects of Coenzyme Q10 against Hyperglycemia-Mediated Oxidative Stress by Focusing on Nrf2/Keap1/HO-1 Signaling Pathway in the Liver of Diabetic Rats.

Fatemeh Samimi, Maryam Baazm, Zahra Nadi, Sanaz Dastghaib, Mehri Rezaei, Farideh Jalali-Mashayekhi

Abstract read
In one paragraph

Article in Iranian journal of medical sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Optimized CoQ10 deliveryRSC advances · 2026
    Article
  3. Review
  4. Article
  5. Coenzyme Q10 and Intracellular Signalling Pathways: Clinical Relevance.International journal of molecular sciences · 2025
    Review
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Fatemeh SamimiDepartment of Biochemistry and Genetics, School of Medicine, Arak University of Medical Sciences, Arak, Iran.
Maryam BaazmDepartment of Anatomy, School of Medicine, Arak University of Medical Sciences, Arak, Iran.
Zahra NadiDepartment of Anatomy, School of Medicine, Arak University of Medical Sciences, Arak, Iran.
Sanaz DastghaibEndocrinology and Metabolism Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Mehri RezaeiDepartment of Biochemistry and Genetics, School of Medicine, Arak University of Medical Sciences, Arak, Iran.
Farideh Jalali-MashayekhiDepartment of Biochemistry and Genetics, School of Medicine, Arak University of Medical Sciences, Arak, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Hyperglycemia-induced oxidative stress can damage the liver and lead to diabetes complications. Coenzyme Q10 (CoQ-10) reduces diabetes-related oxidative stress. However, its molecular mechanisms are still unclear. This study aimed to examine CoQ-10's antioxidant capabilities against hyperglycemia-induced oxidative stress in the livers of diabetic rats, specifically targeting the Nrf2/Keap1/ARE signaling pathway. Methods: This study was conducted between 2020-2021 at Arak University of Medical Sciences. A total of 30 male adult Wistar rats (8 weeks old) weighing 220-250 g were randomly assigned to five groups (n=6 in each group): control healthy, sesame oil (CoQ-10 solvent), CoQ-10 (10 mg/Kg), diabetic, and diabetic+CoQ-10. Liver oxidative stress indicators, including malondialdehyde, catalase, glutathione peroxidase, and glutathione, were estimated using the spectrophotometry method. Nrf2, Keap1, HO-1, and NQO1 gene expressions were measured using real-time PCR tests in the liver tissue. All treatments were conducted for 6 weeks. Statistical analysis was performed using SPSS software. One-way ANOVA followed by LSD's or Tukey's Results: The findings showed that induction of diabetes significantly increased Keap1 expression (2.1±0.9 folds, P=0.01), and significantly inhibited the mRNA expression of Nrf2 (0.38±0.2 folds, P=0.009), HO-1 (0.27±0.1 folds, P=0.02), and NQO1 (0.26±0.1 folds P=0.01), compared with the healthy group. In the diabetic group, the activity of glutathione peroxidase, catalase enzymes, and glutathione levels was decreased with an increase in malondialdehyde level. CoQ-10 supplementation significantly up-regulated the expressions of Nrf2 (0.85±0.3, P=0.04), HO-1 (0.94±0.2, P=0.04), NQO1 (0.88±0.5, P=0.03) genes, and inhibited Keap1 expression (1.1±0.6, P=0.02). Furthermore, as compared to control diabetic rats, CoQ-10 ameliorated oxidative stress by decreasing malondialdehyde levels and increasing catalase, glutathione peroxidase activities, and glutathione levels in the liver tissues of the treated rats in the treatment group. Conclusion: The findings of this study revealed that CoQ-10 could increase the antioxidant capacity of the liver tissue in diabetic rats by modulating the Nrf2/Keap1/HO-1/NQO1 signaling pathway.

Indexed as

AntioxidantsDiabetes Mellitus, ExperimentalKelch-Like ECH-Associated Protein 1LiverNF-E2-Related Factor 2Oxidative StressSignal TransductionUbiquinoneAnimalsHeme Oxygenase (Decyclizing)HyperglycemiaMaleRatsRats, WistarAntioxidantscoenzyme Q10Heme Oxygenase (Decyclizing)Hmox1 protein, ratKEAP1 protein, ratKelch-Like ECH-Associated Protein 1Nfe2l2 protein, ratNF-E2-Related Factor 2UbiquinoneCoenzyme Q10Diabetes mellitusNrf2/Keap1/ARE pathwayOxidative stressRats

Identifiers

PMID39449772
PMCPMC11497326

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.