• IMMUNE NETWORK
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• v.23 no.5
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• pp.38.1-38.14
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• 2023

Neutrophils are professional phagocytes that provide defense against invading pathogens through phagocytosis, degranulation, generation of ROS, and the formation of neutrophil extracellular traps (NETs). Although long been considered as short-lived effector cells with limited biosynthetic activity, recent studies have revealed that neutrophils actively communicate with other immune cells. Neutrophils employ various types of soluble mediators, including granules, cytokines, and chemokines, for crosstalk with immune cells. Additionally, ROS and NETs, major arsenals of neutrophils, are utilized for intercellular communication. Furthermore, extracellular vesicles play a crucial role as mediators of neutrophil crosstalk. In this review, we highlight the extracellular mechanisms of neutrophils and their roles in crosstalk with other cells.

• Proceedings of the Zoological Society Korea Conference
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• 2000.10a
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• pp.195.2-196
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• 2000

No Abstract, See Full Text

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.156.2-156.2
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• 2002

• Korean Journal of Plant Resources
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• v.26 no.2
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• pp.227-233
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• 2013

This study was carried out to effects of Allium victorials extract on lowering lipid, anti-oxidation and concentration of inflammatory mediators in rats fed high oxidized fat. Concentration of free fatty acid(FFA), triglyceride(TG), total cholesterol and LDL-cholesterol in plasma decreased in the Allium victorials extract groups and plasma HDL-cholesterol concentration revealed a tendency to increase in Allium victorials extract groups. Concentration of total cholesterol and TG in liver showed a tendency to decrease in Allium victorials extract groups. Concentration of thiobarbituric acid(TBARS) in plasma and liver showed a lower values in Allium victorials extract groups than that of control group. Activities of glutathione peroxidase(GSH-Px), superoxide dismutase(SOD) and catalase(CAT) in liver showed a tendency to increase in Allium victorials extract groups. Concentration of nitrogen oxide(NO), ceruloplasmin and ${\alpha}1$-acid glycoprotein in plasma showed a lower values in Allium victorials extract groups than that of control group. These results indicate that the Allium victorials extract have an functional material for lowering lipid, anti-oxidation and anti-inflammatory effect.

• IMMUNE NETWORK
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• v.8 no.1
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• pp.13-20
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• 2008

Background: Coptis chinensis rhizome has been used as a medicinal herb in traditional Oriental medicine. We investigated the effects of Coptis chinensis extract on inflammatory mediators and delayed type hypersensitivity in mice. Methods: The inhibitory effect of ethanolic extract of Coptis chinensis (CCE) on cell proliferation was evaluated using MTS assay. The lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and the Con A-activated mouse splenocytes were cultured with various concentrations of CCE. Total nitric oxide (NO) production was determined by Griess reaction. The amounts of secreted prostaglandine E2 ($PGE_2$), interleukin (IL)-2 and IFN-${\gamma}$ were measured by ELISA. To investigate the in vivo anti-inflammatory effect of CCE, oxazolone-induced delayed type hypersensitivity (DTH) model was used. Results: The CCE at $100{\mu}g/ml$ significantly blocked the LPS-induced production of pro-inflammatory mediators (NO and PGE) in RAW264.7 macrophages. Also, it significantly inhibited cell proliferation and cytokine (IL-2 and IFN-${\gamma}$) production in splenocytes. Furthermore, when splenocytes from CCE fed mice (200 mg/kg for 2 weeks) were activated with Con A, cell proliferation and cytokine production were significantly inhibited. In addition, CCE decreased in vivo inflammation in oxazolone-induced DTH model mice. Conclusion: We suggest that Coptis chinensis can be used as an anti-inflammatory drug by exerting an inhibitory effect in inflammatory mediator- and cell-mediated inflammation.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.2
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• pp.653-664
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• 2012

Objective: This study assessed anti-inflammatory and antioxidant activities of $E.$ $foetidum$ leaf extract on LPS-activated murine macrophages. Methods: RAW264.7 cells were pretreated with or without $E.$ $foetidum$ extract for 1 h prior to incubation with LPS for 24 h. Anti-inflammatory activity was evaluated with reference to iNOS, COX-2, TNF-${\alpha}$ and IL-6 gene expression. In addition, NO and intracellular ROS generation were determined by Griess method and fluorescence intensity and activation of MAPKs and $I{\kappa}B$ by Western blotting. Results: Prior treatment with $E.$ $foetidum$ leaf extract inhibited elevation of IL-6, TNF-${\alpha}$, iNOS and COX-2, together with their cognate mRNAs in a dose-dependent manner. NO and intracellular ROS contents were similarly reduced. These effects were due to inhibition of LPS-induced phosphorylation of JNK and p38 as well as $I{\kappa}B$. $E.$ $foetidum$ ethanol extract were shown to contain lutein, ${\beta}$-carotene, chlorogenic acid, kaempferol and caffeic acid, compounds known to exert these bioactive properties. Conclusions: $E.$ $foetidum$ leaf extract possesses suppressive effects against pro-inflammatory mediators. Thus, $E.$ $foetidum$ has a high potential to be used as a food supplement to reduce risk of cancer associated with inflammation.

• The Korea Journal of Herbology
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• v.30 no.5
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• pp.67-74
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• 2015

Objectives : TheHaedokgumhwa-sanwater extract (HDKHS) is used in Korea, Japan and China as a traditional therapeutic agent to cure an infectious disease. But its study is not enough. Therefore, the present study focused on the elucidation of HDKHS to investigate the anti-inflammatory effects and to established the possible mechanisms involved in its action on LPS-stimulated immune response in murine macrophages.Methods : Inflammatory status was induced by LPS and measured by increasement of inflammatory mediators. LPS induced secretions of NO and PGE₂in RAW 264.7 cells were measured using griess reagent and enzyme-linked immunosorbent assay (ELISA) kit respectively. production of IL-6 was examined using ELISA kit and expression of IL-6 mRNA was measured by RT-PCR method. To investigate the effects of HDKHS on inflammatory mediators, such as iNOS, COX-2 and MAPKs, western blot and RT-PCR were performed.Results : HDKHS significantly reduced production of NO and PGE2 which were induced by LPS. Also, activation of IL-6 was reduced both protein and mRNA levels. The expressions of inflammatory mediator include iNOS and COX-2 were decreased by pretreatment with HDKHS. futhermore The result showed HDKHS down-regulate the LPS induced phosphorylation of ERK 1/2, one of the MAPK family, which is considered as a main regulator of transmission from pathogens to nucleus of immune cells.Conclusions : Our results suggest that the anti-inflammatory properties of HDKHS may stem from the inhibition of pro-inflammatory mediators via suppression of initiation of inflammatory response by inhibiting MAPKs signaling pathways.

• BMB Reports
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• v.48 no.3
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• pp.172-177
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• 2015

Upregulation of pro-inflammatory mediators contributes to ${\beta}$-cell destruction and enhanced infiltration of immune cells into pancreatic islets during development of type 1 diabetes mellitus. In this study, we examined the regulatory effects and the mechanisms of action of celastrol against cytotoxicity and pro-inflammatory immune responses in the RINm5F rat pancreatic ${\beta}$-cell line stimulated with a combination of interleukin-1 beta, tumor necrosis factor-alpha, and interferon-${\gamma}$. Celastrol significantly restored cytokine-induced cell death and significantly inhibited cytokine-induced nitric oxide production. In addition, the protective effect of celastrol was correlated with a reduction in pro-inflammatory mediators, such as inducible nitric oxide synthase, cyclooxygenase-2, and CC chemokine ligand 2. Furthermore, celastrol significantly suppressed cytokine-induced signaling cascades leading to nuclear factor kappa B (NF-${\kappa}B$) activation, including $I{\kappa}B$-kinase (IKK) activation, $I{\kappa}B$ degradation, p65 phosphorylation, and p65 DNA binding activity. These results suggest that celastrol may exert its cytoprotective activity by suppressing cytokine-induced expression of pro-inflammatory mediators by inhibiting activation of NF-${\kappa}B$ in RINm5F cells.

• Biomolecules & Therapeutics
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• v.21 no.5
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• pp.381-390
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• 2013

The purpose of this study was to examine whether ginsenoside Rg3 (GRg3) could improve learning and memory impairments and inflammatory reactions induced by injecting lipopolysaccharide (LPS) into the brains of rats. The effects of GRg3 on proinflammatory mediators in the hippocampus and the underlying mechanisms of these effects were also investigated. Injection of LPS into the lateral ventricle caused chronic inflammation and produced deficits in learning in a memory-impairment animal model. Daily administration of GRg3 (10, 20, and 50 mg/kg, i.p.) for 21 consecutive days markedly improved the LPS-induced learning and memory disabilities demonstrated on the step-through passive avoidance test and Morris water maze test. GRg3 administration significantly decreased expression of pro-inflammatory mediators such as tumor necrosis factor-${\alpha}$, interleukin-1${\beta}$, and cyclooxygenase-2 in the hippocampus, as assessed by reverse transcription-polymerase chain reaction analysis and immunohistochemistry. Together, these findings suggest that GRg3 significantly attenuated LPS-induced cognitive impairment by inhibiting the expression of pro-inflammatory mediators in the rat brain. These results suggest that GRg3 may be effective for preventing or slowing the development of neurological disorders, including Alzheimer's disease, by improving cognitive and memory functions due to its anti-inflammatory activity in the brain.

• Microbiology and Biotechnology Letters
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• v.43 no.2
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• pp.158-163
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• 2015

In this study, we investigated the effects of 40% ethanol extract of Red Ginseng (RGE) on the productions of inflammatory proteins in Antigen I/II (Ag I/II)-N, a recombinant protein isolated from Streptococcus mutans -stimulated in RAW 264.7 cells. RGE inhibited the expression of Ag I/II-N-induced pro-inflammatory mediators, both mRNA and protein synthesis levels, without any cytotoxic effects. Moreover, RGE significantly inhibited Ag I/II-N induced NF-κB translocation into the nucleus by preventing the degradation of inhibitor κB-α. In conclusion, RGE down regulates the expression of pro-inflammatory genes involved in the synthesis of NO and iNOS in Ag I/II-N-stimulated RAW 264.7 cells by suppressing NF-κB activity.