ArticleFrontiers in pharmacology2023
Exploring the molecular mechanism of notoginsenoside R1 in sepsis-induced cardiomyopathy based on network pharmacology and experiments validation.
Article in Frontiers in pharmacology, 2023. 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, 17 citations in OpenAlex.
- Mechanisms ofFood science & nutrition · 2026Article
- Identification and validation of MYC as an autophagy-related gene for diagnosis and immune infiltration in sepsis-induced myocardial dysfunction.Journal of cardiothoracic surgery · 2026Article
- Visual analysis of research status and hotspots of Panax notoginseng from 2000 to 2023: A bibliometric review.Medicine · 2026Review
- Cell-free DNA in sepsis: from molecular insights to clinical management.Military Medical Research · 2025Review
- Notoginsenoside R1 Attenuates H/R Injury in H9c2 Cells by Maintaining Mitochondrial Homeostasis.Current issues in molecular biology · 2025Article
- Optimization of saponin extraction from the leaves ofFood chemistry: X · 2024Article
- Enhancing the inhibition of cell proliferation and induction of apoptosis in H22 hepatoma cells through biotransformation of notoginsenoside R1 byRSC advances · 2023Article
- Research Progress on the Mechanism and Management of Septic Cardiomyopathy: A Comprehensive Review.Emergency medicine international · 2023Review
- The U-Shaped Relationship Between Serum Bicarbonate Levels and 28-Day Mortality in Patients With Sepsis: A Retrospective Cohort Study of MIMIC-IV Database.Dose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-induced cardiomyopathy (SIC) is an important manifestation of sepsis, and abnormal cardiac function affects the development of sepsis. Notoginsenoside R1 (NG-R1) is a unique bioactive component of Panax notoginseng with anti-inflammatory and antioxidant effects. However, the effects and possible mechanisms of NG-R1 on SIC are not clear. The purpose of this study was to identify the potential targets and regulatory mechanisms of the action of NG-R1 on SIC. To investigate the potential mechanism, we used network pharmacology, molecular docking, qRT-PCR, and immunofluorescence. The results showed that NG-R1 ameliorated myocardial fibrosis in septic mice. Validation of network pharmacology and molecular docking results revealed that NG-R1 reduced tumor necrosis factor-Alpha (TNF-α) expression in myocardial tissues and AC16 cardiomyocytes in mice, as well as inflammatory factor release in AC16 cells, so TNF-α may be a potential target of NG-R1 against SIC. The present study demonstrated that NG-R1 could protect against SIC and by regulating the expression of TNF-α inflammatory factors, providing a new idea for sepsis drug development.
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