ArticleKorean journal of anesthesiology2015
Propofol attenuates hydrogenperoxide-induced apoptosis in human umbilical vein endothelial cells via multiple signaling pathways.
Article in Korean journal of anesthesiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- The Influence of Anesthetics on the Functions of the Endothelium and Oxidative Stress: A Critical Review.Biomedicines · 2025Review
- Propofol protects cardiomyocytes from doxorubicin-induced toxic injury by activating the nuclear factor erythroid 2-related factor 2/glutathione peroxidase 4 signaling pathways.Bioengineered · 2022Article
- Propofol induces mitochondrial-associated protein LRPPRC and protects mitochondria against hypoxia in cardiac cells.PloS one · 2020Article
- The protective role of DMBT1 in cervical squamous cell carcinoma.The Kaohsiung journal of medical sciences · 2019Article
- Pink Urine Syndrome: A Combination of Insulin Resistance and Propofol.Kidney international reports · 2019Review
- Propofol inhibits cell proliferation and invasion in rheumatoid arthritis fibroblast-like synoviocytes via the nuclear factor-κB pathway.American journal of translational research · 2017Article
- Anesthetic Propofol-Induced Gene Expression Changes in Patients Undergoing Coronary Artery Bypass Graft Surgery Based on Dynamical Differential Coexpression Network Analysis.Computational and mathematical methods in medicine · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPropofol has been reported to protect vascular endothelial cells against oxidative stress. In this study we investigated its effect on hydrogen peroxide (H2O2)-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and examined the possible signaling pathways.
methodsHUVECs were pretreated with propofol (1, 5, 25, and 50 µM) for 30 min and then co-incubated with 0.4 mM H2O2 for 4 h. Cell viability was assessed using a Cell Counting Kit-8. Cell apoptosis was analyzed using flow cytometry with annexin V/propidium iodide staining, and evaluated by quantifying caspase-3, Bax, and Bcl-2 expression levels. The expression levels of p38 mitogen activated protein kinase (MAPK), phosphorylated (p)-p38 MAPK, cJun-N-terminal kinases (JNK), phosphorylated (p)-JNK, Akt and phosphorylated Akt [(p)-Akt] (Ser473) were measured by western blotting.
resultsH2O2 treatment induced the activation of caspase-3, downregulated Bcl-2 expression, and up-regulated Bax expression, all of which were dose-dependently attenuated by propofol pretreatment. Furthermore, propofol significantly ameliorated H2O2-induced phosphorylation of p38 MAPK, JNK, and Akt in HUVECs.
conclusionsPropofol can protect HUVECs against H2O2-induced apoptosis via a mechanism that may involve p38 MAPK, JNK, and Akt signaling pathways.
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