ArticleJournal of arrhythmia2017
Catechin and epicatechin reduce mitochondrial dysfunction and oxidative stress induced by amiodarone in human lung fibroblasts.
Article in Journal of arrhythmia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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.
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.
Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- Cocoa flavanols, Nrf2 activation, and oxidative stress in peripheral artery disease: mechanistic findings in muscle based on outcomes from a randomized trial.American journal of physiology. Cell physiology · 2024Trial
- The protective effect of chemical and natural compounds against amiodarone induced toxicity: A systematic review.Biochemistry and biophysics reports · 2026Review
- Systems Pharmacology and Multitarget Modulation of Letrozole-HFD-Induced Polycystic Ovarian Syndrome by Fruit Pulp of Prunus armeniaca.Chemistry & biodiversity · 2026Article
- Article
- Artemisinin protected human bronchial epithelial cells from amiodarone-induced oxidative damage via 5'-AMP-activated protein kinase (AMPK) activation.Redox report : communications in free radical research · 2025Article
- Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions.Cell biochemistry and biophysics · 2025Review
- A Combined Extract fromAntioxidants (Basel, Switzerland) · 2024Article
- Green tea catechin prevents oxidative stress-regulated autophagy and apoptosis signaling, and inhibits tenderness in postmortem bovineFood chemistry: X · 2023Article
- Article
- Mitochondrial Modulators: The Defender.Biomolecules · 2023Review
- Mitochondrion-targeted RNA therapies as a potential treatment strategy for mitochondrial diseases.Molecular therapy. Nucleic acids · 2022Review
- Hydrophilic Scaffolds Containing Extracts ofPharmaceutics · 2022Article
- Review
- Phenolic Characterization Using cLC-DAD Analysis and Evaluation of In Vitro and In Vivo Pharmacological Activities ofAntioxidants (Basel, Switzerland) · 2022Article
- Effects of catechin on a rodent model of autism spectrum disorder: implications for the role of nitric oxide in neuroinflammatory pathway.Psychopharmacology · 2021Article
- Cell-Permeable Succinate Rescues Mitochondrial Respiration in Cellular Models of Amiodarone Toxicity.International journal of molecular sciences · 2021Article
- Dietary Cocoa Flavanols Enhance Mitochondrial Function in Skeletal Muscle and Modify Whole-Body Metabolism in Healthy Mice.Nutrients · 2021Article
- Bioactive Components, Volatile Profile and In Vitro Antioxidative Properties ofMolecules (Basel, Switzerland) · 2021Article
- Modulatory effects of catechin hydrate on benzo[a]pyrene-induced nephrotoxicity in adult male albino rats.Toxicology research · 2021Article
- Grape seed proanthocyanidins improves mitochondrial function and reduces oxidative stress through an increase in sirtuin 3 expression in EA.hy926 cells in high glucose condition.Molecular biology reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAmiodarone (AMD) and its metabolite N-desethylamiodarone can cause some adverse effects, which include pulmonary toxicity. Some studies suggest that mitochondrial dysfunction and oxidative stress may play a role in these adverse effects. Catechin and epicatechin are recognized as important phenolic compounds with the ability to decrease oxidative stress. Therefore, the aim of this study was to evaluate the potential of catechin and epicatechin to modulate mitochondrial dysfunction and oxidative damage caused by AMD in human lung fibroblast cells (MRC-5).
methodsMitochondrial dysfunction was assessed through the activity of mitochondrial complex I and ATP biosynthesis. Cell viability was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Superoxide dismutase and catalase activity were measured spectrophotometrically at 480 and 240 nm, respectively. Lipid and protein oxidative levels were determined by thiobarbituric reactive substances and protein carbonyl assays, respectively. Nitric oxide (NO) levels were evaluated using the Griess reaction method.
resultsAMD was able to inhibit the activity of mitochondrial complex I and ATP biosynthesis in MRC-5 cells. Lipid and protein oxidative markers increased along with cell death, while superoxide dismutase and catalase activities and NO production decreased with AMD treatment. Both catechin and epicatechin circumvented mitochondrial dysfunction, thereby restoring the activity of mitochondrial complex I and ATP biosynthesis. Furthermore, the phenolic compounds were able to restore the imbalance in superoxide dismutase and catalase activities as well as the decrease in NO levels induced by AMD. Protein and lipid oxidative damage and cell death were reduced by catechin and epicatechin in AMD-treated cells.
conclusionsCatechin and epicatechin reduced mitochondrial dysfunction and oxidative stress caused by AMD in MRC-5 cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.