ArticleExperimental and therapeutic medicine2020
Catalpol ameliorates doxorubicin-induced inflammation and oxidative stress in H9C2 cells through PPAR-γ activation.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Sotagliflozin ameliorates doxorubicin-induced cardiomyopathy by regulating inflammation and mitochondrial dysfunction through the AMPK/mTOR pathway.Experimental and therapeutic medicine · 2026Article
- Mechanism study of miR-324-3p driving myocardial infarction progression through regulation of myocardial inflammation.Journal of cardiothoracic surgery · 2026Article
- Article
- Catalpol: an natural multifunctional iridoid glycoside with promising therapeutic properties.Frontiers in molecular biosciences · 2026Review
- Preventive Effect of Protocatechuic Acid Ethyl Ester against Doxorubicin-Induced Toxicity in Cardiomyocytes.International journal of preventive medicine · 2026Article
- Limitations of Ferroptosis Inhibitors on the Doxorubicin-Induced Cardiotoxicity.Antioxidants (Basel, Switzerland) · 2025Article
- Catalpol: An Iridoid Glycoside With Potential in Combating Cancer Development and Progression-A Comprehensive Review.Phytotherapy research : PTR · 2025Review
- Catalpol inhibits Hedgehog signaling pathway to suppress proliferation and promote lipid accumulation in rat meibomian gland epithelial cells.Cytotechnology · 2025Article
- The Gut-Heart Axis and Its Role in Doxorubicin-Induced Cardiotoxicity: A Narrative Review.Microorganisms · 2025Review
- Potential benefits of Rehmanniae Radix after ancient rice-steaming process in promotion of antioxidant activity in rats' health.Food science & nutrition · 2023Article
- Lactate Can Modulate the Antineoplastic Effects of Doxorubicin and Relieve the Drug's Oxidative Damage on Cardiomyocytes.Cancers · 2023Article
- Doxorubicin-induced acute cardiotoxicity is associated with increased oxidative stress, autophagy, and inflammation in a murine model.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Activation of NR1H3 attenuates the severity of septic myocardial injury by inhibiting NLRP3 inflammasome.Bioengineering & translational medicine · 2023Article
- Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy.Cell communication and signaling : CCS · 2023Review
- Article
- Exogenous 8-hydroxydeoxyguanosine attenuates doxorubicin-induced cardiotoxicity by decreasing pyroptosis in H9c2 cardiomyocytes.BMC molecular and cell biology · 2022Article
- The attenuation effect of low piperinePharmaceutical biology · 2022Article
- Targeting PPARs Signaling Pathways in Cardiotoxicity by Natural Compounds.Cardiovascular toxicology · 2022Review
- MiR-24-3p Attenuates Doxorubicin-induced Cardiotoxicity via the Nrf2 Pathway in Mice.Current medical science · 2022Article
- Feasibility of Catalpol Intranasal Administration and Its Protective Effect on Acute Cerebral Ischemia in Rats via Anti-Oxidative and Anti-Apoptotic Mechanisms.Drug design, development and therapy · 2022Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug-induced cardiomyopathy is a severe disease that leads to refractory heart disease at late stages, with increasing detrimental effects. DOX-induced cell damage is primarily induced via cellular oxidative stress. The present study investigated the effects of catalpol on doxorubicin (DOX)-induced H9C2 cardiomyocyte inflammation and oxidative stress. The Cell Counting Kit-8 assay was performed to detect cell viability, and western blotting was performed to detect the expression of peroxisome proliferator-activated receptor (PPAR)-γ in H9C2 cells. The expression levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 were measured using ELISAs. Furthermore, the oxidative stress kit was used to detect the levels of malondialdehyde, superoxide dismutase and glutathione peroxidase. A reactive oxygen species (ROS) kit and DCF-DA staining were used to detect ROS levels. The results indicated that DOX treatment inhibited H9C2 cell expression of PPAR-γ and decreased H9C2 cell viability. Various concentrations of catalpol exhibited a less potent effect on H9C2 cell viability compared with DOX; however, catalpol increased the viability of DOX-induced H9C2 cells. Catalpol treatment also significantly decreased the expression levels of inflammatory factors (TNF-α, IL-1β and IL-6) in DOX-induced H9C2 cells, which was reversed by transfections with short hairpin RNA targeting PPAR-γ. Results from the present study indicated that catalpol ameliorated DOX-induced inflammation and oxidative stress in H9C2 cardiomyoblasts by activating PPAR-γ.
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