Effect of propofol on generation of inflammatory mediator of monocytes

Nie, Yiming; Lu, Yan-Xi; Lv, Li-Hong

doi:10.1016/j.apjtm.2015.10.008

Cited by 5 publications

(6 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LPS stimulation can induce HMGB1 release from mouse macrophages, however, propofol can inhibit this process leading to downregulation of HMGB1 mRNA and also block the activation of nuclear transcription factor-κB (NF-κB) [ 10 ]. In addition, the propofol can inhibit the expression of toll-like receptor 4 (TLR-4) and NF-κB to block the activation of p38 mitogen-activated protein kinase and the expression of pro-inflammatory cytokines [ 4 ]. However, the actions of propofol to regulate the expressions of interleukin-6 (IL-6), 8 (IL-8) and TNF-α and the correlation with HMGB1 in LPS-stimulated murine macrophage are unclear.…”

Section: Introductionmentioning

confidence: 99%

Propofol inhibits the release of interleukin-6, 8 and tumor necrosis factor-α correlating with high-mobility group box 1 expression in lipopolysaccharides-stimulated RAW 264.7 cells

Jia

Sun

et al. 2017

BMC Anesthesiol

View full text Add to dashboard Cite

BackgroundStudies have found that propofol can inhibit endotoxin-induced monocyte-macrophages to produce various inflammatory factors. This study is to disclose whether the propofol affects the expression of high-mobility group box 1 (HMGB1) in lipopolysaccharides (LPS)-stimulated RAW 264.7 cells and the release of interleukin-6 (IL-6), 8 (IL-8) and tumor necrosis factor-α (TNF-α).MethodsRAW 264.7 cells were divided into four groups for intervention. After culturing for 16 h, the cells and culture supernatants were collected. The expression of HMGB1 in RAW 264.7 cells was detected by Western blot. The levels of IL-6, IL-8 and TNF-α in supernatants of cells were determined by enzyme-linked immunosorbent assay (ELISA).ResultsStimulation of LPS increased the expression of HMGB1 and promoted the release of IL-6, IL-8 and TNF-α in supernatants of RAW 264.7 cells (p < 0.05); however, propofol down-regulated the expression of LPS-stimulated HMGB1 and reduced the LPS-stimulated releases of IL-6, IL-8 and TNF-α in supernatants of RAW 264.7 cells (p < 0.05). Moreover, the releases of IL-6, IL-8 and TNF-α intimately correlated with the expression of HMGB1 in this process (p < 0.05).ConclusionPropofol inhibited the releases of IL-6, IL-8 and TNF-α in LPS-stimulated RAW 264.7 cells, and the levels of IL-6, IL-8 and TNF-α intimately correlated with the expression of HMGB1, which indicating that propofol may prevent inflammatory responses through reducing the releases of these cytokines and inflammatory mediators.

show abstract

Section: Introductionmentioning

confidence: 99%

Propofol inhibits the release of interleukin-6, 8 and tumor necrosis factor-α correlating with high-mobility group box 1 expression in lipopolysaccharides-stimulated RAW 264.7 cells

Jia

Sun

et al. 2017

BMC Anesthesiol

View full text Add to dashboard Cite

show abstract

“…Activation of p38 MAPK signaling induces the expression of pro-inflammatory mediators, including COX-2 and tumor necrosis factor-α (TNF-α) [ 20 21 22 ]. Measurement of p38 phosphorylation levels in the blood monocytes of mice with endotoxemia revealed that LPS can induce p38 phosphorylation; propofol treatment could significantly inhibit p38 phosphorylation, indicating that propofol has an anti-inflammatory effect [ 8 ]. Furthermore, propofol was shown to inhibit p38 MAPK phosphorylation in alveolar epithelial cells and cardiomyocytes [ 20 23 ].…”

Section: Discussionmentioning

confidence: 99%

“…Propofol is an intravenous anesthetic commonly used for general anesthesia and sedation owing to its rapid onset of action and short recovery time [ 8 ]. In recent studies, propofol has been shown to have anti-inflammatory effects in vitro as well as in vivo .…”

Section: Introductionmentioning

confidence: 99%

“…Toll-like receptor 4 (TLR4) is a pattern recognition receptor for LPS. Binding of LPS to TLR4 during the LPS-induced inflammatory response activates MAPK and nuclear factor-kappa B (NF-κB) signaling pathways [ 8 10 11 ]. LPS also enhances the production of cyclooxygenase-2 (COX-2), which is essential for prostaglandin E 2 (PGE 2 ) production [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells

Kim

Lee

Yoon

et al. 2022

J Dent Anesth Pain Med

View full text Add to dashboard Cite

Background Nonobstetric surgery is sometimes required during pregnancy, and neck abscess or facial bone fracture surgery cannot be postponed in pregnant women. However, dental surgery can be stressful and can cause inflammation, and the inflammatory response is a well-known major cause of preterm labor. Propofol is an intravenous anesthetic commonly used for general anesthesia and sedation. Studies investigating the effect of propofol on human amnion are rare. The current study investigated the effects of propofol on lipopolysaccharide (LPS)-induced inflammatory responses in human amnion-derived WISH cells. Methods WISH cells were exposed to LPS for 24 h and co-treated with various concentrations of propofol (0.01–1 µg/ml). Cell viability was measured using the MTT assay. Nitric oxide (NO) production was analyzed using a microassay based on the Griess reaction. The protein expression of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE 2), p38, and phospho-p38 was analyzed using western blotting. Results Propofol did not affect the viability and NO production of WISH cells. Co-treatment with LPS and propofol reduced COX-2 and PGE 2 protein expression and inhibited p38 phosphorylation in WISH cells. Conclusion Propofol does not affect the viability of WISH cells and inhibits LPS-induced expression of inflammatory factors. The inhibitory effect of propofol on inflammatory factor expression is likely mediated by the inhibition of p38 activation.

show abstract

“…Over the past few decades, several researchers have reported its protective effects in ischemic-reperfusion injury, including cerebral ischemic injury. Most of these reports attributed propofol's neuroprotective effect to its anti-inflammatory (Nie et al, 2015 ; Samir et al, 2015 ) and antioxidant (Ucar et al, 2015 ; Hsiao et al, 2016 ) properties. However, in the clinical setting, propofol is often administered to patients with an intact central nervous system (CNS).…”

Section: Introductionmentioning

confidence: 99%

Profiling of Long Non-coding RNAs and mRNAs by RNA-Sequencing in the Hippocampi of Adult Mice Following Propofol Sedation

Fan

Zhou

et al. 2018

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Propofol is a frequently used intravenous anesthetic agent. The impairment caused by propofol on the neural system, especially the hippocampus, has been widely reported. However, the molecular mechanism underlying the effects of propofol on learning and memory functions in the hippocampus is still unclear. In the present study we performed lncRNA and mRNA analysis in the hippocampi of adult mice, after propofol sedation, through RNA-Sequencing (RNA-Seq). A total of 146 differentially expressed lncRNAs and 1103 mRNAs were identified. Bioinformatics analysis, including gene ontology (GO) analysis, pathway analysis and network analysis, were done for the identified dysregulated genes. Pathway analysis indicated that the FoxO signaling pathway played an important role in the effects of propofol on the hippocampus. Finally, four lncRNAs and three proteins were selected from the FoxO-related network for further validation. The up-regulation of lncE230001N04Rik and the down-regulation of lncRP23-430H21.1 and lncB230206L02Rik showed the same fold change tendencies but changes in Gm26532 were not statistically significant in the RNA-Seq results, following propofol sedation. The FoxO pathway-related proteins, PI3K and AKT, are up-regulated in propofol-exposed group. FoxO3a is down-regulated at both mRNA and protein levels. Our study reveals that propofol sedation can influence the expression of lncRNAs and mRNAs in the hippocampus, and bioinformatics analysis have identified key biological processes and pathways associated with propofol sedation. Cumulatively, our results provide a framework for further study on the role of lncRNAs in propofol-induced or -related neurotoxicity, particularly with regards to hippocampus-related dysfunction.

show abstract

Effect of propofol on generation of inflammatory mediator of monocytes

Abstract: The propofol can inhibit the expression of TLR-4 and NF-κB to inhibit the activation of p38 and the expression of pro-inflammatory cytokines.

Cited by 5 publications

References 16 publications

Propofol inhibits the release of interleukin-6, 8 and tumor necrosis factor-α correlating with high-mobility group box 1 expression in lipopolysaccharides-stimulated RAW 264.7 cells

Propofol inhibits the release of interleukin-6, 8 and tumor necrosis factor-α correlating with high-mobility group box 1 expression in lipopolysaccharides-stimulated RAW 264.7 cells

Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells

Profiling of Long Non-coding RNAs and mRNAs by RNA-Sequencing in the Hippocampi of Adult Mice Following Propofol Sedation

Contact Info

Product

Resources

About