ArticleLaboratory investigation; a journal of technical methods and pathology2021
Tubeimoside I improves endothelial function in sepsis via activation of SIRT3.
Article in Laboratory investigation; a journal of technical methods and pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Pathological mechanisms and clinical research progress of endothelial dysfunction.Frontiers in cardiovascular medicine · 2026Review
- β-Nicotinamide Mononucleotide Alleviates Sepsis-associated Acute Kidney Injury by Activating NAD+/SIRT3 Signaling.Cell biochemistry and biophysics · 2025Article
- Advances in the treatment of lower-extremity ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- The role and therapeutic potential of SIRTs in sepsis.Frontiers in immunology · 2024Review
- Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3.Oxidative medicine and cellular longevity · 2023Article
- Mitochondrial Sirt3 serves as a biomarker for sepsis diagnosis and mortality prediction.Scientific reports · 2022Article
- Chinese endemic medicinal plantFrontiers in pharmacology · 2022Review
- Tubeimoside I Ameliorates Myocardial Ischemia-Reperfusion Injury through SIRT3-Dependent Regulation of Oxidative Stress and Apoptosis.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is life-threatening organ dysfunction caused by a deregulated host response to infection. Endothelial dysfunction is the initial factor leading to organ dysfunction and it is associated with increased mortality. There is no effective drug to treat sepsis-induced endothelial dysfunction. In this study, we detected a favorable effect of tubeimoside I (TBM) in ameliorating sepsis-induced endothelial dysfunction. To unveil the mechanism how TBM protects against sepsis-induced endothelial dysfunction, we examined TBM's effects on oxidative stress and apoptosis both in vivo and in vitro. TBM treatment alleviated oxidative stress by decreasing NOX2 and Ac-SOD2/SOD2 and decreased apoptosis by inhibiting cleaved caspse3 and Bax/Bcl-2. Notably, sepsis induced a significant decrease of SIRT3 expression in vascular endothelium, while TBM treatment reversed SIRT3 expression. To clarify whether TBM provides protection via SIRT3, we knockdown SIRT3 using siRNA before TBM treatment. Then, the cytoprotective effects of TBM were largely abolished by siSIRT3. This suggests that SIRT3 plays an essential role in TBM's endothelial protective effects and TBM might be a potential drug candidate to treat sepsis-induced endothelial dysfunction.
Indexed as
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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.