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Materials And Methods: Bark extracts of these plants (1 and 25 g/mL) were added 3 hours before coincubating H9c2 cardiomyoblasts with Dox (0.5 and 1 M) for 24 hours more. We measured cell mass and metabolic viability, mitochondrial transmembrane potential, superoxide anion content, and activity-like of caspase-3 and caspase-9 following treatment with the extracts and/or Dox. Also, selenium and vitamin C contents were measured in the plant extracts.
Results: The results confirmed that Dox treatment decreased cell mass, mitochondrial membrane potential and metabolic viability, increased mitochondrial superoxide anion, and stimulated caspase-3 and caspase-9-like activities. Pretreatment of the cells with the plant extracts significantly inhibited Dox cytotoxicity, with more significant results at the higher concentration. Measurements of selenium and vitamin C in the extracts revealed higher concentration of both when compared with other Cameroonian spices.
Conclusion: Both extracts of and were effective against Dox-induced cytotoxicity, most likely due to their content in antioxidants.
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http://dx.doi.org/10.1155/2021/8858165 | DOI Listing |
Adv Med Sci
September 2025
Chair and Department of Medical Microbiology, Medical University of Lublin, Lublin, Poland. Electronic address:
Purpose: The aim of the study was to evaluate the toxicity of triclosan in the Danio rerio model and mammalian cells, as well as to assess its antimicrobial and antibiofilm activity against selected bacterial pathogens.
Methods: Triclosan toxicity was assessed in Danio rerio embryos in accordance with OECD Test Guideline 236: Fish Embryo Acute Toxicity (FET) Test. Cytotoxicity was evaluated in vitro using the MTT assay on human dermal fibroblasts (BJ) and rat cardiomyoblasts (H9c2).
Transpl Immunol
September 2025
Department of Cardiovascular Medicine, Tianjin Medical University General Hospital, Tianjin City 300000, PR China. Electronic address:
Background: Myocardial ischemia/reperfusion (I/R) injury is a common cause of death. FXYD domain-containing ion transport regulator-5 (Fxyd5) is a type I membrane protein that plays a significant role in mediating cellular functions. However, the expression and function of Fxyd5 in myocardial I/R injury remain unclear.
View Article and Find Full Text PDFIran J Basic Med Sci
January 2025
Department of Liver and Gallbladder Surgery, Jiangjin District Central Hospital of Chongqing, Chongqing, 402260, China.
Objectives: This study aimed to investigate the cardioprotective effects of lycopene loaded ovalbumin chitosan nanoparticle (L-OCNPs) against isoproterenol (ISO)-induced myocardial injury.
Materials And Methods: H9c2 cardiomyoblasts were treated with various concentrations of L-OCNPs (5, 10, 15, 25, and 50 µg/ml) for 24 hr, followed by exposure to ISO (100 µM) for an additional 24 hr. Cell viability, oxidative stress, mitochondrial function, and nuclear damage were assessed using various biochemical and molecular techniques.
Int J Mol Sci
August 2025
Institute for Heart Research, Centre of Experimental Medicine, Slovak Academy of Sciences, Dúbravská cesta 9, 84104 Bratislava, Slovakia.
This study investigates the role of sulforaphane (SFN) and quercetin (QCT) in alleviating the oxidative stress and modulation of cellular responses induced by doxorubicin (DOX) in rat cardiomyoblast cells H9c2. The potential mechanisms involving Wnt/β-catenin signaling and antioxidant response were determined. We found that SFN effectively mitigated DOX-induced cytotoxicity in H9c2 cells.
View Article and Find Full Text PDFJ Ginseng Res
September 2025
The Key Laboratory of Fujian Province Universities on Ion Channel and Signal Transduction in Cardiovascular Diseases, The School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian, China.
Background: Myocardial hypertrophy is a crucial pathological change that occurs during post-anthracycline treatment cardiomyopathy. The effects of ginsenoside Rb1 (Rb1) on anthracycline-induced hypertrophy remain unclear. This study aimed to explore the antihypertrophic effect of Rb1 on post-doxorubicin (DOX) treatment myocardial hypertrophy and underlying mechanism.
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