Propofol inhibits lipoteichoic acid-induced iNOS gene expression in macrophages possibly through downregulation of toll-like receptor 2-mediated activation of Raf-MEK1/2-ERK1/2-IKK-NFκB

Effect of dexmedetomidine, midazolam, and propofol on lipopolysaccharide‑stimulated dendritic cells

“…Though the inhibit effect of propofol on cytokine were similar seen in many previous study, our study shows that propofol could enhanced LPS-induced COX2, that may be because of the difference cells. As antigen-processing and presenting cells, activation of DCs in inflammation was earlier than others in their study, like macrophage and microglia (30)(31)(32). Moreover, the concentration of propofol based on clinical blood concentration in our study was lower than the study on DC (33).…”

Anesthetic Propofol Causes Glycogen Synthase Kinase-3β-regulated Lysosomal/Mitochondrial Apoptosis in Macrophages

“…8,11,53,54 Mechanistic studies showed that the molecular mechanism for propofol-conferred antiinflammatory status is generally targeted on nuclear factor-kappa B (NF-B) activation. [55][56][57][58] In addition, propofol also decreases lipopolysaccharide-or lipoteichoic acidactivated MAPK/ERK, an upstream regulator of NF-B nuclear translocation. 57,58 In this study, we found that propofol overdose disrupts phagocytic activities, which is consistent with the previous studies that propofol represses the biologic function of phagocytes.…”

“…[55][56][57][58] In addition, propofol also decreases lipopolysaccharide-or lipoteichoic acidactivated MAPK/ERK, an upstream regulator of NF-B nuclear translocation. 57,58 In this study, we found that propofol overdose disrupts phagocytic activities, which is consistent with the previous studies that propofol represses the biologic function of phagocytes. 16 Notably, the mechanisms for the inhibitory effects are down-regulation of mitochondrial activities and the induction of lysosomal/mitochondrial apoptotic pathways.…”

“…Finally, further investigation showed that propofol overdose inactivates p70 S6K and ERK but not ILK and p38 MAPK, which are both negative regulators for GSK-3␤. 29 -38 The possible mechanisms for propofol-induced downregulation of Akt, p70 S6K, and ERK are currently under investigation while there are reports showing that propofol decreases ERK for antiinflammation 57,58 and for neuron cell death. 18 In conclusion, using an in vitro model of propofol overdoseinduced apoptosis in macrophages, we define the proapoptotic signaling of propofol through inactivating GSK-3␤-regulating kinases Akt.…”

Propofol Attenuates Lipopolysaccharide-Induced Monocyte Chemoattractant Protein-1 Production Through Enhancing apoM and foxa2 Expression in HepG2 Cells

“…Inflammation involves permeability changes in vascular walls leading to enhanced movement of immune cells from the vascular lumen into the tissues [7]. Propofol reduces the release of inflammatory mediators, such as interleukin-6 and tumor necrosis factor alpha, and inhibits the production of reactive oxygen species (ROS) by phagocytic cells, neutrophil chemotaxis, cellular attachment and migration, phagocytosis, and platelet aggregation [8][9][10]. Furthermore, our group recently reported that propofol inhibited lipopolysaccharide (LPS)-induced production of pro-inflammatory cytokines and this anti-inflammatory effect might be mediated through apolipoprotein M (apoM) in a hepatocyte nuclear factor 1 alpha (HNF-1α)-dependent manner [11].…”