ArticleFood & nutrition research2018
3,5-Dicaffeoylquinic acid protects H9C2 cells against oxidative stress-induced apoptosis via activation of the PI3K/Akt signaling pathway.
Article in Food & nutrition research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Chlorogenic Acid: A Systematic Review on the Biological Functions, Mechanistic Actions, and Therapeutic Potentials.Nutrients · 2024Pooled it
- Comparative Phytochemical and Antiviral Characteristics ofPlants (Basel, Switzerland) · 2026Article
- GC-Ms, UHPLC-MS/MSChemistry & biodiversity · 2026Article
- Linking Experimental Models to Pathophysiology: Oxidative Stress and DNA Damage in Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- The Underlying Pharmacological Mechanisms and Active Components of XZZTP in Modulating Bacterial Inflammation Elucidated by LC-MS/MS, Network Pharmacology, In Vitro Experiments, Molecular Docking, and Dynamics Simulations.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Article
- Advances in Pharmacological Properties, Molecular Mechanisms, and Bioavailability Strategies of Chlorogenic Acid in Cardiovascular Diseases Therapy.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Pristimerin Dampens Acetaminophen-Induced Hepatotoxicity; The Role of NF-κB/iNOS/COX-II/Cytokines, PI3K/AKT, and BAX/BCL-2/Caspase-3 Signaling Pathways.Pharmaceutics · 2025Article
- Article
- Pharmacological advances of the chlorogenic acids family: current insights and future research directions.Frontiers in pharmacology · 2025Review
- 3,5-diCQA suppresses colorectal cancer cell growth through ROS/AMPK/mTOR mediated mitochondrial dysfunction and ferroptosis.Cell cycle (Georgetown, Tex.) · 2023Article
- Plumbagin protects H9c2 cardiomyocytes against TBHP-induced cytotoxicity by alleviating ROS-induced apoptosis and modulating autophagy.Experimental and therapeutic medicine · 2022Article
- Profiling of Polyphenolic Compounds ofPlants (Basel, Switzerland) · 2021Article
- 3,5-Dicaffeoylquinic Acid Lowers 3T3-L1 Mitotic Clonal Expansion and Adipocyte Differentiation by Enhancing Heme Oxygenase-1 Expression.Molecules (Basel, Switzerland) · 2021Article
- Transcriptomic analysis reveals the role of a peptide derived from CRYAB on the CoClJournal of thrombosis and thrombolysis · 2021Article
- Downregulated MicroRNA-327 Attenuates Oxidative Stress-Mediated Myocardial Ischemia Reperfusion Injury Through Regulating the FGF10/Akt/Nrf2 Signaling Pathway.Frontiers in pharmacology · 2021Article
- Tanshinone I Inhibits Oxidative Stress-Induced Cardiomyocyte Injury by Modulating Nrf2 Signaling.Frontiers in pharmacology · 2021Article
- Neuroprotective Effects of Methyl Caffeate against Hydrogen Peroxide-Induced Cell Damage: Involvement of Caspase 3 and Cathepsin D Inhibition.Biomolecules · 2020Article
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Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOxidative stress-induced apoptosis plays an important role in the development of heart failure. 3,5-Dicaffeoylquinic acid (3,5-diCQA), a phenolic compound, has shown protective effects against oxidative stress in many diseases.
objectiveThe objective of this study was to investigate the anti-apoptosis potential of 3,5-diCQA in cardiomyocyte cells under oxidative stress and explore its underlying mechanisms.
designA model of tert-butyl hydroperoxide (TBHP)-induced apoptosis in a cardiomyocyte cell line (H9C2) was established. Cell viabilities on cell lines were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium (MTT) assay. The apoptosis was measured by hoechst33342 and propidium iodide (PI) fluorescent staining. PI (in red) stained the regions of cell apoptosis; Hoechet33342 (in blue) stained the nuclei. The Western blot was used to determine the expressions of related proteins such as p-PI3K: phosphorylated phosphatidylinositol-3-kinase (p-PI3K), phosphorylated Serine and Threonine kinase AKT (p-AKT), p-PTEN, Bcl-2, Bax, and caspase-3. Afterward, a PI3K inhibitor, LY294002, was applied to confirm the influence of the PI3K/Akt pathway on TBHP-treated cells of 3,5-diCQA. Then, H9C2 cells were pre-incubated with 3,5-diCQA alone to determine if the expression of activated PI3K/Akt signaling was mediated by 3,5-diCQA in H9C2 cells.
resultsThe results showed that TBHP resulted in an increase in cardiomyocyte apoptosis, whereas 3,5-diCQA treatment protected cells from TBHP-induced apoptosis in a dose-dependent manner. Moreover, 3,5-diCQA decreased expressions of Bax and caspase-3 but increased the phosphorylation levels of PI3K and Akt in TBHP-treated cells, which are the key molecules mediating cell survival, whereas phosphatase and tensin homologue deleted on chromosome 10 (PTEN) phosphorylation was unchanged. Importantly, pre-incubation with a PI3K inhibitor (LY294002) partly abolished the anti-apoptosis effects of 3,5-diCQA. Further, 3,5-diCQA enhanced the phosphorylation levels of PI3K and Akt in H9C2 cells directly, while LY294002 attenuated the effects of 3,5-diCQA on PI3K and Akt.
conclusionThis study suggested that 3,5-diCQA rescued myocardium from apoptosis by increasing the activation of the PI3K/Akt signaling pathway.
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