ArticlePloS one2011
Propofol inhibits the activation of p38 through up-regulating the expression of annexin A1 to exert its anti-inflammation effect.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 49 citations in OpenAlex.
- Effects of propofol on the inflammatory response during robot-assisted laparoscopic radical prostatectomy: a prospective randomized controlled study.Scientific reports · 2019Trial
- Immunomodulatory effects of total intravenous and balanced inhalation anesthesia in patients with bladder cancer undergoing elective radical cystectomy: preliminary results.Journal of experimental & clinical cancer research : CR · 2013Trial
- Mesenchymal stem cell derived exosomes mitigate COVID-19 cytokine storm via Annexin A1 and TGF-β mediated MAPK pathway inhibition.Stem cell research & therapy · 2026Article
- Mild hypothermia combined with dexmedetomidine reduced brain, lung, and kidney damage in experimental acute focal ischemic stroke.Intensive care medicine experimental · 2022Article
- Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells.Journal of dental anesthesia and pain medicine · 2022Article
- Article
- Propofol suppresses adipose-derived stem cell progression via PI3K/AKT-Wnt signaling pathway.BMC anesthesiology · 2022Article
- Intermittent Hypoxia and Atherosclerosis: From Molecular Mechanisms to the Therapeutic Treatment.Oxidative medicine and cellular longevity · 2022Review
- Annexin A1 restores cerebrovascular integrity concomitant with reduced amyloid-β and tau pathology.Brain : a journal of neurology · 2021Article
- Effects of propofol on hippocampal neuron viability.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2020Article
- Annexin A1 accounts for an anti-inflammatory binding target of sesamin metabolites.NPJ science of food · 2020Article
- Propofol attenuates TNF-α-induced MMP-9 expression in human cerebral microvascular endothelial cells by inhibiting CaActa pharmacologica Sinica · 2019Article
- Effect of Propofol on the Production of Inflammatory Cytokines by Human Polarized Macrophages.Mediators of inflammation · 2019Article
- Propofol Alleviates Apoptosis Induced by Chronic High Glucose Exposure via Regulation of HIF-1Oxidative medicine and cellular longevity · 2019Article
- Pilose antler polypeptide protects against sevoflurane‑mediated neurocyte injury.Molecular medicine reports · 2018Article
- Propofol protects against endotoxin-induced myocardial injury by inhibiting NF-κB-mediated inflammation.Experimental and therapeutic medicine · 2018Article
- The resolution of acute inflammation induced by cyclic AMP is dependent on annexin A1.The Journal of biological chemistry · 2017Article
- Differential role of intravenous anesthetics in colorectal cancer progression: implications for clinical application.Oncotarget · 2016Article
- Posttreatment with propofol attenuates lipopolysaccharide-induced up-regulation of inflammatory molecules in primary microglia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Propofol inhibits lipopolysaccharide-induced tumor necrosis factor-alpha expression and myocardial depression through decreasing the generation of superoxide anion in cardiomyocytes.Oxidative medicine and cellular longevity · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory response is a kind of nonspecific immune response, with the central link of vascular response, which is mainly manifested by changes in neutrophils and vascular endothelial cells. In recent years, the in vivo and in vitro role of intravenous anesthetic propofol in inhibiting inflammatory response has been attracting more and more attention, but the anti-inflammatory mechanisms of propofol for mononuclear cells still remain undefined. In this study, proteomics analysis was applied to investigate protein expression profile changes in serum mononuclear cells following intervention of rats with endotoxemia using propofol. After two-dimensional electrophoresis and mass spectrometric identification, it has been found that the protein Annexin A1 was up-regulated in the propofol intervention group. Annexin A1 is a glucocorticoid-dependent anti-inflammatory protein. After detection using ELISA and Western blot assays, it has also been found that propofol can not only promote the expression of Annexin A1, but also inhibit the phosphorylation level of p38 and release of inflammatory factors (IL-1β, IL-6 and TNF-α) in rats with endotoxemia. In order to further determine the role of up-regulated expression of Annexin A1 in anti-inflammation of propofol, this gene was silenced in vitro in human THP-1 cells, to detect the phosphorylation status of p38 and release of inflammatory factors. The results show that Annexin A1 can negatively regulate phosphorylation of p38 and release of IL-1β, IL-6 and TNF-α in THP-1 cells following propofol intervention and lipopolysaccharide (LPS) stimulation. Our results clearly indicate that propofol can up-regulate Annexin A1 to inhibit the phosphorylation level of p38 and release of IL-1β, IL-6 and TNF-α, so as to inhibit inflammatory response. Therefore, it can be speculated that Annexin A1 might be the key signaling protein in the in vivo and in vitro anti-inflammatory mechanisms of propofol.
Indexed as
Identifiers
What OpenQuestion holds
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.