ArticleBioscience reports2020
Myc is involved in Genistein protecting against LPS-induced myocarditis in vitro through mediating MAPK/JNK signaling pathway.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Genistein - A Broad-spectrum Bioactive Compound with Diverse Pharmacological Potential: A Systematic Review.Current molecular medicine · 2026Pooled it
- Multidimensional targeting of ischemia-reperfusion injury by genistein: from molecular crosstalk to clinical translation.Frontiers in pharmacology · 2026Review
- Qing-Xin-Jie-Yu granule prevents myocardial infarction-induced apoptosis via inhibition of p38 MAPK pathway.Frontiers in cardiovascular medicine · 2026Article
- Pharmacological Effects of Genistein on Cardiovascular Diseases.Evidence-based complementary and alternative medicine : eCAM · 2023Review
- Hypoxia-inducible transcription factor-1α inhibition by topotecan protects against lipopolysaccharide-induced inflammation and apoptosis of cardiomyocytes.Biomedical engineering online · 2021Article
- Network Pharmacology Combined with Bioinformatics to Investigate the Mechanisms and Molecular Targets ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Fulminant myocarditis: a comprehensive review from etiology to treatments and outcomes.Signal transduction and targeted therapy · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGenistein is widely used as a pharmacological compound as well as a food additive. However, the pharmaceutical effects of Genistein on myocarditis and its potential mechanisms have not been studied in detail.
methodsH9c2 cells were continuously stimulated by lipopolysaccharide (LPS) for 12 h to simulate the in vitro model of myocarditis injury. DrugBank, String, and GEO dataset were used to investigate specific genes that interacting with Genistein. KEGG and GO enrichment analysis were employed to explore Myc-related signaling pathways. Biological behaviors of H9c2 cells were observed with the support of cell counting kit-8, MTT and flow cytometry. Expression levels of cytokines including TNF-α and ILs were evaluated by enzyme-linked immunosorbent assay. Western blot was applied to detect the expression of Myc and MAPK pathway related proteins.
resultsGenistein alleviated the damage of H9c2 cells subjected to LPS from the perspective of elevating cells growth ability, and inhibiting cells apoptosis and inflammatory response. Through bioinformatics analysis, we identified Myc as the potential target of Genistein in myocarditis, and MAPK as the signaling pathway. Significantly, Myc was highly up-regulated in myocarditis samples. More importantly, by performing biological experiments, we discovered that Genistein relieved H9c2 cells apoptosis and inflammatory reaction which caused by LPS stimulation through inhibiting Myc expression. Additionally, the marked augmentation of p-P38 MAPK and p-JNK expression in LPS-induced cardiomyocyte model were blocked by Genistein and si-Myc.
conclusionsOur research revealed that Myc mediated the protective effects of Genistein on H9c2 cells damage caused by LPS partly through modulation of MAPK/JNK signaling pathway.
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