ArticleMolecular biotechnology2024
Effect of L-carnitine in Ameliorating Lipopolysaccharide-Induced Cardiomyocyte Injury via MAPK Signaling.
Article in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Mechanistic attenuation by L-carnitine of trastuzumab-induced downregulation of adenosine monophosphate -activated protein kinase signal in cardiac H9c2 cells.BMC pharmacology & toxicology · 2026Article
- HDAC1-mediated SUCLA2 lysine β-hydroxybutyrylation modulates myocardial mitochondrial function in sepsis-induced heart dysfunction.Redox biology · 2026Article
- Translational selenium nanoparticles trigger apoptosis in triple-negative breast cancer cells through the MAPKs/Bcl2 pathway.Bioactive materials · 2026Article
- Comprehensive review of the expanding roles of the carnitine pool in metabolic physiology: beyond fatty acid oxidation.Journal of translational medicine · 2025Review
- The Role of Mitochondrial Dysfunction and Inflammatory Response in the Pathogenesis of Sepsis-Induced Myocardial Injury: A Mechanistic Study.Journal of inflammation research · 2025Review
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Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to elucidate whether L-carnitine (LC) protected H9c2 cells and its underlying mechanisms. Cell counting kit-8 (CCK-8) assay was used to evaluate cell viability. Apoptosis, cell morphology, and lactate dehydrogenase (LDH) assessment were used to prove effects of lipopolysaccharide (LPS) and LC on H9c2 cells. RT-qPCR and western blot assays were hired to evaluate the mRNA and protein expression levels, respectively. ELISA assay was performed to determine the released protein levels. Reactive oxygen species (ROS) level was evaluated by immunofluorescence and flow cytometry. LC was revealed to protect H9c2 cells against LPS-induced injury as indicated by increased cell viability, reduced apoptosis ratio and LDH level. LC treatment also reduced BAX expression as well as up-regulated Bcl-2 expression under LPS treatment. Mechanically, LC reduced oxidative stress and ameliorated the mitochondrial injury through modulating extracellular signal-regulated kinase 1/2 and c-Jun N-terminal protein kinase c-Jun N-terminal protein kinase phosphorylation levels as indicated by decreased membrane potential, increased ATP production and mtDNA expression. We found that LC ameliorates LPS-induced cardiomyocyte injury by abrogating cell apoptosis ratio, ROS levels, as well as mitochondrial dysfunction via mitogen-activated protein kinase signaling. Our findings revealed a potential drug for sepsis or LPS-induced cardiomyocyte injury.
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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.