ArticleDose-response : a publication of International Hormesis Society
Mechanism of Metformin on LPS-Induced Bacterial Myocarditis.
Article in Dose-response : a publication of International Hormesis Society. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Metformin improves endotoxemia and alters folliculogenesis in women with polycystic ovary syndrome.Endocrine connections · 2026Article
- Cardioprotective Effect of Metformin Treatment in Mouse Model of Experimental Autoimmune Myocarditis.Cardiovascular therapeutics · 2026Article
- Targeting ATF4-DDIT4/TXNIP induced mitochondrial dysfunction and ferroptosis: ISRIB as novel therapy for septic cardiomyopathy.Journal of translational medicine · 2025Article
- Comparison of the Protective Effects of Nebivolol and Metoprolol against LPS-Induced Injury in H9c2 Cardiomyoblasts.Current issues in molecular biology · 2023Article
- Puerarin protects against sepsis-induced myocardial injury through AMPK-mediated ferroptosis signaling.Aging · 2022Article
- Mono-macrophage-Derived MANF Alleviates Bacterial Myocarditis by Inhibiting NF-kappaB Activation and Myocardial Inflammation.Inflammation · 2021Article
- Hypoxia-inducible transcription factor-1α inhibition by topotecan protects against lipopolysaccharide-induced inflammation and apoptosis of cardiomyocytes.Biomedical engineering online · 2021Article
- Myc is involved in Genistein protecting against LPS-induced myocarditis in vitro through mediating MAPK/JNK signaling pathway.Bioscience reports · 2020Article
- Protective Effect of Metformin on Sepsis Myocarditis in Zebrafish.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
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Authors and funding
7 authors.
Funding
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Abstract
aimsMetformin is commonly used to treat type 2 diabetes mellitus; however, in recent years, it was found to play a potential role in the protection of myocardial injury. In this study, we intended to investigate whether metformin had protective effects on bacterial myocarditis. METHODS AND
resultsWe stimulated rat cardiac myoblast H9c2 cells with lipopolysaccharide (LPS) and administrated with metformin. The results showed that cell viability after LPS stimulation was greatly reduced. The expression levels of phosphorylated p38 mitogen-activated protein kinases (MAPK) and c-Jun N-terminal kinases (JNK), nuclear factor (NF)-κB (NF-κB), BAX, and cleaved Caspase3 were significantly increased, while the expression of antiapoptotic protein Bcl-2 showed a prominent decrease compared to control. Nevertheless, the cells activity increased remarkably after metformin administration, and the expression levels of intracellular related proteins showed the opposite trend to that of the LPS group.
conclusionWe demonstrate that LPS stimulation may activate intracellular MAPK/JNK and NF-κB signaling pathways and thus induce cell apoptosis. In contrast, metformin reduced apoptosis by inhibiting this signaling pathway and increasing the expression level of Bcl-2. Moreover, it was found that metformin could enhance the ability of cells to antagonize redox damage by regulating the activities of superoxide dismutase and lactate dehydrogenase and subsequently promote the recovery of cardiomyocyte function.
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