ArticleOxidative medicine and cellular longevity2014
Propofol inhibits lipopolysaccharide-induced tumor necrosis factor-alpha expression and myocardial depression through decreasing the generation of superoxide anion in cardiomyocytes.
Article in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Natural products as multi‑target therapies for sepsis‑induced myocardial dysfunction (Review).International journal of molecular medicine · 2026Review
- Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy.Experimental and therapeutic medicine · 2023Article
- Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells.Journal of dental anesthesia and pain medicine · 2022Article
- Propofol improves brain injury induced by chronic cerebral hypoperfusion in rats.Food science & nutrition · 2021Article
- Dulaglutide Alleviates LPS-Induced Injury in Cardiomyocytes.ACS omega · 2021Article
- Propofol ameliorates endotoxin‑induced myocardial cell injury by inhibiting inflammation and apoptosis via the PPARγ/HMGB1/NLRP3 axis.Molecular medicine reports · 2021Article
- Hydrogen Sulfide Attenuated Sepsis-Induced Myocardial Dysfunction Through TLR4 Pathway and Endoplasmic Reticulum Stress.Frontiers in physiology · 2021Article
- Rutin Prevents LTA Induced Oxidative Changes in H9c2 Cells.Preventive nutrition and food science · 2020Article
- [Molecular mechanism underlying the inhibitory effect of propofol on lipopolysaccharide-induced pyroptosis of mouse bone marrow-derived macrophages].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- NADPH Oxidase Hyperactivity Contributes to Cardiac Dysfunction and Apoptosis in Rats with Severe Experimental Pancreatitis through ROS-Mediated MAPK Signaling Pathway.Oxidative medicine and cellular longevity · 2019Article
- HS3ST1 genotype regulates antithrombin's inflammomodulatory tone and associates with atherosclerosis.Matrix biology : journal of the International Society for Matrix Biology · 2017Article
- Activation of Endocannabinoid Receptor 2 as a Mechanism of Propofol Pretreatment-Induced Cardioprotection against Ischemia-Reperfusion Injury in Rats.Oxidative medicine and cellular longevity · 2017Article
- Differential role of intravenous anesthetics in colorectal cancer progression: implications for clinical application.Oncotarget · 2016Article
- Propofol attenuates LPS-induced tumor necrosis factor-α, interleukin-6 and nitric oxide expression in canine peripheral blood mononuclear cells possibly through down-regulation of nuclear factor (NF)-κB activation.The Journal of veterinary medical science · 2015Article
- Expert consensus on the perioperative management of patients with sepsis.World journal of emergency medicine · 2015Article
- Mechanical Ventilation Induces an Inflammatory Response in Preinjured Lungs in Late Phase of Sepsis.Oxidative medicine and cellular longevity · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TNF-α has been shown to be a major factor responsible for myocardial depression in sepsis. The aim of this study was to investigate the effect of an anesthetic, propofol, on TNF-α expression in cardiomyocytes treated with LPS both in vivo and in vitro. In cultured cardiomyocytes, compared with control group, propofol significantly reduced protein expression of gp91phox and phosphorylation of extracellular regulated protein kinases 1/2 (ERK1/2) and p38 MAPK, which associates with reduced TNF-α production. In in vivo mice studies, propofol significantly improved myocardial depression and increased survival rate of mice after LPS treatment or during endotoxemia, which associates with reduced myocardial TNF-α production, gp91phox, ERK1/2, and p38 MAPK. It is concluded that propofol abrogates LPS-induced TNF-α production and alleviates cardiac depression through gp91phox/ERK1/2 or p38 MAPK signal pathway. These findings have great clinical importance in the application of propofol for patients enduring sepsis.
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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.