ArticleNeuroreport2018
Delayed treatment of propofol inhibits lipopolysaccharide-induced inflammation in microglia through the PI3K/PKB pathway.
Article in Neuroreport, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Mechanisms of Action of Propofol in Modulating Microglial Activation in Ischemic Stroke.Molecules (Basel, Switzerland) · 2025Review
- Research progress of propofol in alleviating cerebral ischemia/reperfusion injury.Pharmacological reports : PR · 2024Review
- Propofol inhibits neuroinflammation and metabolic reprogramming in microgliaFrontiers in pharmacology · 2023Article
- Identification of Potential Anti-Neuroinflammatory Inhibitors from Antarctic Fungal StrainMolecules (Basel, Switzerland) · 2022Article
- Propofol Regulates the TLR4/NF-κB Pathway Through miRNA-155 to Protect Colorectal Cancer Intestinal Barrier.Inflammation · 2021Article
- Effects of anesthetic agents on inflammation in Caco-2, HK-2 and HepG2 cells.Experimental and therapeutic medicine · 2021Article
- Propofol Inhibits Microglial ActivationFrontiers in cellular neuroscience · 2021Article
- Propofol Suppresses Microglia Inflammation by Targeting TGM2/NF-Journal of immunology research · 2021Article
- Propofol Ameliorates Microglia Activation by Targeting MicroRNA-221/222-IRF2 Axis.Journal of immunology research · 2021Article
- Adult Mild Encephalitis With Reversible Splenial Lesion Associated With Delirious Mania: A Case Report.Frontiers in psychiatry · 2020Article
- Sub-anaesthetic dose of propofol attenuates mechanical allodynia in chronic post-ischaemic painMolecular painArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Propofol is a short-acting intravenous anesthetic agent with potential neuroprotective effect. In this study, we aim to investigate whether delayed propofol treatment is protective against lipopolysaccharide (LPS)-stimulated inflammatory responses in microglial cells. Cultured BV2 microglial cells were exposed to propofol at various time points after initiation of LPS stimulation. Nitrite production and cell viability were assessed after stimulation with LPS for 24 h. The effect of propofol on mRNA levels of cyclooxygenase-2 (Cox-2), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β) was analyzed using reverse transcription PCR (RT-PCR) 6 h after LPS stimulation. The production of TNF-α and reactive oxygen species was also studied. Propofol applied 0-4 h after the initiation of LPS dose-dependently inhibits nitric oxide production. Propofol application also decreased LPS-induced Cox-2, IL-6, iNOS, TNF-α, and IL-1β mRNA expression and induced significant protein kinase B (PKB) phosphorylation in BV2 cells. Treatment with phosphoinositide 3-kinase (PI3K)/PKB inhibitor wortmannin decreased PKB phosphorylation induced by propofol, and abolished the inhibitory effect of propofol on LPS-stimulated NO, reactive oxygen species and TNF-α production. Our results suggest that delayed propofol treatment can reduce LPS-induced activation of microglial cells. These effects may be mediated by activation of the PI3K/PKB pathway.
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