ArticleMolecules (Basel, Switzerland)2015
Tyrosol prevents ischemia/reperfusion-induced cardiac injury in H9c2 cells: involvement of ROS, Hsp70, JNK and ERK, and apoptosis.
Article in Molecules (Basel, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 81 citations in OpenAlex.
- Exploring the Therapeutic Potential ofCurrent issues in molecular biology · 2025Article
- Hypoxic extracellular vesicles from hiPSCs protect cardiomyocytes from oxidative damage by transferring antioxidant proteins and enhancing Akt/Erk/NRF2 signaling.Cell communication and signaling : CCS · 2024Article
- Traditional uses, phytochemistry, pharmacology, toxicity and clinical application of traditional Chinese medicineFrontiers in pharmacology · 2024Review
- Oral administration of nano-tyrosol reversed the diabetes-induced liver damage in streptozotocin-induced diabetic rats.Journal of diabetes and metabolic disorders · 2023Article
- Necrostatin-1 prevents skeletal muscle ischemia reperfusion injury by regulating Bok-mediated apoptosis.Journal of the Chinese Medical Association : JCMA · 2023Article
- Effect of p-Tyrosol on the Process of Left-Ventricular Remodeling in the Long Period after Myocardial Infarction.Bulletin of experimental biology and medicine · 2022Article
- Downregulation of tripartite motif protein 11 attenuates cardiomyocyte apoptosis after ischemia/reperfusion injury via DUSP1-JNK1/2.Cell biology international · 2022Article
- Rhodiola rosea: A Therapeutic Candidate on Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2022Review
- The protective effects ofFrontiers in cardiovascular medicine · 2022Article
- Bag-1L Protects against Cell Apoptosis in an In Vitro Model of Lung Ischemia-Reperfusion Injury through the C-Terminal "Bag" Domain.BioMed research international · 2021Article
- Polyphenolic-Rich Compounds FromFrontiers in pharmacology · 2021Article
- Proteinase‑activated receptor 2 deficiency is a protective factor against cardiomyocyte apoptosis during myocardial ischemia/reperfusion injury.Molecular medicine reports · 2019Article
- Ethanol exposure in prenatal and early postnatal induced cardiac injury in rats: involvement of oxidative stress, Hsp70, ERK 1/2, JNK, and apoptosis in a 3-month follow-up study.Cell stress & chaperones · 2019Article
- Apurinic/apyrimidinic endonuclease/redox factor 1 (APE1) alleviates myocardial hypoxia-reoxygenation injury by inhibiting oxidative stress and ameliorating mitochondrial dysfunction.Experimental and therapeutic medicine · 2019Article
- Article
- Antioxidative Property and Molecular Mechanisms Underlying Geniposide-Mediated Therapeutic Effects in Diabetes Mellitus and Cardiovascular Disease.Oxidative medicine and cellular longevity · 2019Review
- Trichosanthis Pericarpium Aqueous Extract Protects H9c2 Cardiomyocytes from Hypoxia/Reoxygenation Injury by Regulating PI3K/Akt/NO Pathway.Molecules (Basel, Switzerland) · 2018Article
- Simultaneous Preparation of Salidroside andMolecules (Basel, Switzerland) · 2018Article
- Effects of procyanidin on cardiomyocyte apoptosis after myocardial ischemia reperfusion in rats.BMC cardiovascular disorders · 2018Article
- Grape seed proanthocyanidin extract protects lymphocytes against histone-induced apoptosis.PeerJ · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemia-Reperfusion (I/R) injury causes ROS overproduction, creating oxidative stress, and can trigger myocyte death, resulting in heart failure. Tyrosol is an antioxidant abounded in diets and medicine. Our objective was to investigate the protective effect of tyrosol on I/R-caused mortality in H9c2 cardiomyocytes through its influence on ROS, Hsp70, ERK, JNK, Bcl-2, Bax and caspase-8. A simulated I/R model was used, myocytes loss was examined by MTT, and ROS levels were measured using DCFH-DA. Nuclear condensation and caspase-3 activity were assessed by DAPI staining and fluorometric assay. Phosphorylated ERK and JNK were determined by electrochemiluminescent ELISA, and Hsp70, Bcl-2, Bax and caspase-8 were examined by Western blotting. Results show that tyrosol salvaged myocyte loss, inhibited nuclear condensation and caspase-3 activity dose-dependently, indicating its protection against I/R-caused myocyte loss. Furthermore, tyrosol significantly inhibited ROS accumulation and activation of ERK and JNK, augmenting Hsp70 expression. Besides, tyrosol inhibited I/R-induced apoptosis, associated with retained anti-apoptotic Bcl-2 protein, and attenuated pro-apoptotic Bax protein, resulting in a preservation of Bcl-2/Bax ratio. Finally, tyrosol notably decreased cleaved caspase-8 levels. In conclusion, cytoprotection of tyrosol in I/R-caused myocyte mortality was involved with the mitigation of ROS, prohibition of the activation of ERK, JNK and caspase-8, and elevation of Hsp70 and Bcl-2/Bax ratio.
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