ArticleFrontiers in pharmacology2024
Berberine ameliorates septic cardiomyopathy through protecting mitochondria and upregulating Notch1 signaling in cardiomyocytes.
Article in Frontiers in pharmacology, 2024. 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.
- β-Eudesmol Alleviates Inflammatory Injury in Septic Cardiomyopathy Through Enhancing GSK3B Activity to Inhibiting IL-17-Mediated Chemokine Expression.Biochemical genetics · 2026Article
- Berberine suppresses mechanical stretch-induced apoptosis and proliferation in vascular smooth muscle cells via ROS/PDI/Drp1 signaling pathway.Frontiers in pharmacology · 2026Article
- Structure-activity relationships and molecular mechanisms of natural products in sepsis-associated organ dysfunction: a narrative review.Frontiers in pharmacology · 2026Review
- Traditional Chinese medicine for sepsis: advancing from evidence to innovative drug discovery.Critical care (London, England) · 2025Review
- Mitochondria‑derived peptides: Promising microproteins in cardiovascular diseases (Review).Molecular medicine reports · 2025Review
- Pathogenesis and treatment strategies of sepsis-induced myocardial injury: modern and traditional medical perspectives.International journal of biological sciences · 2025Review
- Preventive effect of small molecule active substances on septic cardiomyopathy after abdominal trauma: a systematic review and meta-analysis.Frontiers in pharmacology · 2025Article
- Article
- Copper-Based Nanoparticles for Effective Treatment Against Sepsis-Induced Lung Injury in Mice Model.International journal of nanomedicine · 2024Article
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Authors and funding
10 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Introduction: Septic cardiomyopathy (SCM) arises as a consequence of sepsis-associated cardiovascular dysfunction, for which there is currently no specific targeted therapy available. Previous studies have demonstrated the beneficial therapeutic effect of berberine (BBR) on SCM; however, the underlying mechanisms of action remain unclear. The objective of this is to elucidate how BBR alleviates SCM. Methods: Septic cardiomyopathy rat model was established by performing cecal ligation and puncture (CLP), while a cardiomyocyte injury model was provoked in H9C2 cells using lipopolysaccharide (LPS). Cardiac function was assessed through echocardiography, and myocardial histopathology was examined with hematoxylin-eosin (HE) staining. Cardiomyocyte viability was determined through Cell Counting Kit-8 (CCK8) assay, and measurement of ATP levels was done with an ATP assay kit. Mitochondrial ultrastructure was observed using transmission electron microscopy. Real-time polymerase chain reaction (RT-PCR) and Western blotting were employed to analyze the expression of Notch1 signaling pathway components and downstream molecules in myocardial tissues and cells. Result: Conclusion: BBR improves septic cardiomyopathy by modulating Notch1 signaling to protect myocardial mitochondria.
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