ArticleInflammation2018
Propofol Attenuates Airway Inflammation in a Mast Cell-Dependent Mouse Model of Allergic Asthma by Inhibiting the Toll-like Receptor 4/Reactive Oxygen Species/Nuclear Factor κB Signaling Pathway.
Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
13 citing papers in PubMed, 25 citations in OpenAlex.
- A Comparison of the Effects of Sevoflurane, Propofol, and Propofol Combined with Butorphanol in Suppressing Sufentanil-Induced cough-A Randomized Controlled Trial.Drug design, development and therapy · 2025Trial
- Deficiency of Toll-like receptor 4 attenuates airway inflammation and remodeling in an ovalbumine-induced mouse asthma model.Journal of thoracic disease · 2025Article
- Induction of M1 polarization in BV2 cells by propofol intervention promotes perioperative neurocognitive disorders through the NGF/CREB signaling pathway: an experimental research.International journal of surgery (London, England) · 2025Article
- Toll-like receptor-mediated immune imbalance in asthma: controversies, breakthroughs, and future directions.Frontiers in immunology · 2025Review
- Effect of General Anesthesia Maintenance with Propofol or Sevoflurane on Fractional Exhaled Nitric Oxide and Eosinophil Blood Count: A Prospective, Single Blind, Randomized, Clinical Study on Patients Undergoing Thyroidectomy.Journal of personalized medicine · 2022Article
- MicroRNA-885-3p alleviates bronchial epithelial cell injury induced by lipopolysaccharide via toll-like receptor 4.Bioengineered · 2022Article
- 18β-Glycyrrhetinic acid suppresses allergic airway inflammation through NF-κB and Nrf2/HO-1 signaling pathways in asthma mice.Scientific reports · 2022Article
- Cytokine-Induced JAK2-STAT3 Activates Tissue Regeneration under Systemic or Local Inflammation.International journal of molecular sciences · 2022Article
- Propofol ameliorates ischemic brain injury by blocking TLR4 pathway in mice.Translational neuroscience · 2022Article
- Edaravone alleviated propofol-induced neural injury in developing rats by BDNF/TrkB pathway.Journal of cellular and molecular medicine · 2021Article
- Identification of biomarkers in common chronic lung diseases by co-expression networks and drug-target interactions analysis.Molecular medicine (Cambridge, Mass.) · 2020Article
- FcεRI-HDAC3-MCP1 Signaling Axis Promotes Passive Anaphylaxis Mediated by Cellular Interactions.International journal of molecular sciences · 2019Review
- Expression of suppressor of cytokine signaling 3 (SOCS3) and interleukin-6 (-174-G/C) polymorphism in atopic conditions.PloS one · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Propofol, an intravenous anesthetic agent widely used in clinical practice, is the preferred anesthetic for asthmatic patients. This study was designed to determine the protective effect and underlying mechanisms of propofol on airway inflammation in a mast cell-dependent mouse model of allergic asthma. Mice were sensitized by ovalbumin (OVA) without alum and challenged with OVA three times. Propofol was given intraperitoneally 0.5 h prior to OVA challenge. The inflammatory cell count and production of cytokines in the bronchoalveolar lavage fluid (BALF) were detected. The changes of lung histology and key molecules of the toll-like receptor 4 (TLR4)/reactive oxygen species (ROS)/NF-κB signaling pathway were also measured. The results showed that propofol significantly decreased the number of eosinophils and the levels of IL-4, IL-5, IL-6, IL-13, and TNF-α in BALF. Furthermore, propofol significantly attenuated airway inflammation, as characterized by fewer infiltrating inflammatory cells and decreased mucus production and goblet cell hyperplasia. Meanwhile, the expression of TLR4, and its downstream signaling adaptor molecules--myeloid differentiation factor 88 (MyD88) and NF-κB, were inhibited by propofol. The hydrogen peroxide and methane dicarboxylic aldehyde levels were decreased by propofol, and the superoxide dismutase activity was increased in propofol treatment group. These findings indicate that propofol may attenuate airway inflammation by inhibiting the TLR4/MyD88/ROS/NF-κB signaling pathway in a mast cell-dependent mouse model of allergic asthma.
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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.