Inhibition of inflammatory responses by FC-77, a perfluorochemical, in lipopolysaccharide-treated RAW 264.7 macrophages

Chang, Hung; Kuo, Fu-Chang; Lai, Yuan-Shu; Chou, Tz-Chong

doi:10.1007/s00134-005-2652-y

Cited by 27 publications

(27 citation statements)

References 23 publications

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“…Then, active NF-κB translocates into the nucleus and triggers an induction of iNOS and pro-inflammatory cytokines (26,28). In the present study, we also found that treatment with FC-77 prevented LPS-induced IκB-α degradation in the cytoplasm and NF-κB activation in nuclei, which is similar to our previous study (11). The result further indicates that inhibition of NF-κB activation by FC-77 may be an important mechanism accounting for the suppression of iNOS expression.…”

Section: Discussionsupporting

confidence: 92%

“…In addition to the improvements in pulmonary physiology, an anti-inflammatory activity of perflubron due to inhibition of the production of reactive oxygen species (ROS) and pro-inflammatory cytokines (7 -10) was reported, which may account for its beneficial effect in acute lung injury. Importantly, our previous study demonstrated that FC-77 reduced prostaglandin E 2 formation and cycloxygenase-2 induction in endotoxin-treated macrophages (11). Accordingly, we propose that FC-77 may exhibit an antiinflammatory activity.…”

Section: Introductionmentioning

confidence: 56%

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Liquid Perfluorochemical Inhibits Inducible Nitric Oxide Synthase Expression and Nitric Oxide Formation in Lipopolysaccharide-Treated RAW 264.7 Macrophages

Chang

Lai

et al. 2009

J Pharmacol Sci

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Abstract. Partial liquid ventilation with various types of perfluorocarbon (PFC) has been shown to be beneficial in treating acute lung injury, a clinical outcome that may involve the anti-inflammatory activity of PFC. FC-77 is a type of PFC with relatively higher vapor pressure and evaporative loss than other PFCs during partial liquid ventilation. Overproduction of nitric oxide (NO) by inducible nitric oxide synthase (iNOS) has been proposed to play a crucial role in the pathogenesis of inflammatory diseases. However, whether the iNOS/NO pathway is affected by FC-77 is unknown. Thus, the aim of this study was to investigate whether FC-77 inhibits iNOS expression and NO production in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages. We found that treatment with FC-77 significantly attenuated LPS-induced iNOS expression/activity and production of NO and reactive oxygen species (ROS). FC-77 also attenuated LPS-induced pro-inflammatory cytokine formation, but enhanced interleukin-10 production. Furthermore, the LPS-induced degradation of cytosolic IκB-α and activation of nuclear transcription factor-κB (NF-κB) were also inhibited by FC-77. In conclusion, the present study is the first to demonstrate that FC-77 decreases LPS-induced NO production in macrophages, which may be associated with the suppression of pro-inflammatory cytokines, and ROS production, as well as NF-κB activation. These results also provide a novel explanation for its anti-inflammatory activity.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 56%

Liquid Perfluorochemical Inhibits Inducible Nitric Oxide Synthase Expression and Nitric Oxide Formation in Lipopolysaccharide-Treated RAW 264.7 Macrophages

Chang

Lai

et al. 2009

J Pharmacol Sci

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“…In addition to its ability for carrying and dissolving high levels of oxygen, PFC has shown anti-inflammatory properties both in vivo and in vitro [11,12]. However, the molecular mechanisms regarding the possible effects of PFC on decreasing sustained inflammation in ARDS have not been elucidated.…”

Section: Introductionmentioning

confidence: 98%

Cytoprotection of Perfluorocarbon on PMVECs In Vitro

Wang

Wei

et al. 2012

Inflammation

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Lipopolysaccharide (LPS) can activate endothelial cells and induce inflammatory injury. Toll-like receptor-4 (TLR-4) is integrally involved in LPS signaling and has a requisite role in the activation of nuclear factor (NF)-κB. A number of studies have demonstrated the cytoprotective action of perfluorocarbon (PFC) both in vivo and in vitro, but the exact mechanisms have yet to be elucidated. In this study, we examined in an in vitro model the cytoprotective effect of PFC on LPS-stimulated pulmonary vascular endothelial cells (PMVECs). Intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α), and interleukin-8 (IL-8) were significantly increased in the LPS-stimulated PMVECs groups. The expression of TLR-4 mRNA and protein in LPS groups was markedly increased. Meanwhile, NF-κB was activated. There were no significant effects of PFC alone on any of the factors studied while the coculture group showed significant downregulation of the secretion of ICAM-1, TNF-α, and IL-8; the expression of TLR-4 mRNA; and the activity of NF-κB. LPS can induce PMVEC inflammatory injury via the activation of TLR-4 and subsequent activation of NF-κB. PFC is able to protect PMVECs from LPS-induced inflammatory injury by blocking the initiation of the LPS signaling pathway.

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“…inhibition of inducible nitric oxide synthase, suppression of the COX2-PGE 2 pathway), and we cannot exclude that they have contributed to the observed effects in our study. 37,38 The oxygenation-and anti-inflammatory capacity of PFCs has led to their pre-clinical and clinical evaluation in numerous pathological conditions including shock, brain injury, anemia and cardiac disease. 39 As far as the authors are aware, the present study is the first report on the successful use of PFCs in inflammatory bowel disease.…”

Section: Discussionmentioning

confidence: 99%

Intrarectal administration of oxygenated perfluorodecalin promotes healing of murine colitis by targeting inflammatory hypoxia

Hindryckx

Devisscher

Laukens

et al. 2011

Laboratory Investigation

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Intestinal inflammation is associated with enhanced mucosal hypoxia, which contributes to the ongoing inflammatory process and hampers appropriate mucosal healing. We questioned whether local treatment with an oxygen (O 2 )-carrying and -releasing molecule (oxygenated perfluorodecalin, O 2 -PFD) could positively influence the course of experimental colitis. The impact of intrarectal (IR) treatment with O 2 -PFD was tested using the murine dextran sodium sulfate (DSS)-induced model of distal colitis, both in preventive and therapeutic settings. Colonic mucosal hypoxia was visualized by pimonidazole staining. Colonic permeability was evaluated with FITC-dextran. In the preventive study, mice treated with O 2 -PFD were protected against DSS colitis compared with saline-treated mice, as demonstrated by reduced shortening of colon length, reduced colonic tumor necrosis factor-alpha levels and a lower histological inflammation score (Po0.05 for all parameters). In the therapeutic study, administration of O 2 -PFD resulted in accelerated recovery of colitis compared with saline-treated littermates, and this was reflected by a better weight evolution, lower myeloperoxidase activity and a lower histological inflammation score (Po0.05 for all parameters). It was found that O 2 -PFD established its therapeutic effects through (1) intrinsic anti-inflammatory effects of the PFD molecule and (2) O 2 -induced preservation and healing of the intestinal epithelial surface. Further in vitro and in vivo studies showed that the barrier-protective activity of O 2 -PFD was obtained through prevention of colonocyte apoptosis and stimulation of colonocyte proliferation during inflammatory hypoxia. These data show that IR treatment with O 2 -PFD promotes colitis healing by the combined actions of direct anti-inflammatory effects and O 2 -induced restitution of the epithelial barrier. As such, O 2 -PFD enemas could be an attractive treatment option for patients with distal inflammatory bowel disease.

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Inhibition of inflammatory responses by FC-77, a perfluorochemical, in lipopolysaccharide-treated RAW 264.7 macrophages

Abstract: FC-77 inhibits inflammatory responses in LPS-stimulated macrophages by a mechanism that involves the attenuation of NF-kappaB dependent induction of COX-2/PGE2 pathway and the pro- /anti-inflammatory cytokine ratio.

Cited by 27 publications

References 23 publications

Liquid Perfluorochemical Inhibits Inducible Nitric Oxide Synthase Expression and Nitric Oxide Formation in Lipopolysaccharide-Treated RAW 264.7 Macrophages

Liquid Perfluorochemical Inhibits Inducible Nitric Oxide Synthase Expression and Nitric Oxide Formation in Lipopolysaccharide-Treated RAW 264.7 Macrophages

Cytoprotection of Perfluorocarbon on PMVECs In Vitro

Intrarectal administration of oxygenated perfluorodecalin promotes healing of murine colitis by targeting inflammatory hypoxia

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