• 제목/요약/키워드: mediators

검색결과 1,402건 처리시간 0.026초

Extracellular Mechanisms of Neutrophils in Immune Cell Crosstalk

  • Sanjeeb Shrestha;Chang-Won Hong
    • IMMUNE NETWORK
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    • 제23권5호
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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.

산마늘추출물이 과산화지질급여 비만쥐의 지질강하, 항산화효과 및 염증매개물질의 생산에 미치는 영향 (Effects of Allium victorials Extract on Lowing Lipid, Anti-oxidation and Concentration of Inflammatory Mediators in Rats Fed High Oxidized Fat)

  • 이은
    • 한국자원식물학회지
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    • 제26권2호
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    • pp.227-233
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    • 2013
  • 본 연구는 산마늘추출물이 과산화지질을 급여한 비만쥐의 지질강하, 항산화효과 및 염증매개물질의 생산에 미치는 영향을 검토했다. 그 결과 혈장 FFA, TG, total cholesterol 및 LDL-cholesterol 농도는 산마늘추출물 처리군 들에서 감소했으며, 혈장HDL-cholesterol 농도는 산마늘추출물 처리군 들에서 증가했다. 간장 내 total cholesterol 농도 및 TG 농도는 산마늘추출물 처리군 들에서 감소하는 경향을 나타내었다. 혈장 및 간장의 TBARS 농도는 산마늘추출물 처리군 모두가 대조군보다 낮은 경향을 보였다. 간장 GSH-Px, SOD 및 CAT활성치모두가 산마늘추출물 처리군 들에서 증가하는 경향을 보였다. 혈장 NO, Ceruloplasmin 및 ${\alpha}1$-acid glycoprotein 농도는 산마늘추출물 투여군 들이 대조군보다 낮은 경향을 나타내었다. 이와 같은 결과는 산마늘추출물에 지질강하, 항산화 및 항염증작용에 효과를 나타내는 기능성물질이 내재하고 있음을 시사한다.

Coptis chinensis Extract Inhibits the Production of Inflammatory Mediators and Delayed Type Hypersensitivity in Mice

  • Lee, Yeon-Ah;Hong, Seung-Jae;Lee, Sang-Hoon;Kim, Kyoung-Soo;Park, Eun-Kyung;Jung, Ki-Won;Han, Chung-Soo;Yoo, Myung-Chul;Yang, Hyung-In
    • IMMUNE NETWORK
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    • 제8권1호
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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.

Eryngium foetidum Suppresses Inflammatory Mediators Produced by Macrophages

  • Mekhora, Chusana;Muangnoi, Channarong;Chingsuwanrote, Pimjai;Dawilai, Suwitcha;Svasti, Saovaros;Chasri, Kaimuk;Tuntipopipat, Siriporn
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권2호
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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.

해독금화산 물추출물이 LPS로 유도된 대식세포의 염증반응에 미치는 영향 (Effects of Haedokgumhwa-san Water Extracts on LPS-induced Inflammatory Response in Macrophage)

  • 임재수;강옥화;서윤수;권동렬
    • 대한본초학회지
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    • 제30권5호
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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.

Celastrol ameliorates cytokine toxicity and pro-inflammatory immune responses by suppressing NF-κB activation in RINm5F beta cells

  • Ju, Sung Mi;Youn, Gi Soo;Cho, Yoon Shin;Choi, Soo Young;Park, Jinseu
    • BMB Reports
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    • 제48권3호
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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.

Ginsenoside Rg3 Alleviates Lipopolysaccharide-Induced Learning and Memory Impairments by Anti-Inflammatory Activity in Rats

  • Lee, Bombi;Sur, Bongjun;Park, Jinhee;Kim, Sung-Hun;Kwon, Sunoh;Yeom, Mijung;Shim, Insop;Lee, Hyejung;Hahm, Dae-Hyun
    • Biomolecules & Therapeutics
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    • 제21권5호
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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.

홍삼에탄올추출물의 염증유발인자에 대한 억제효과 (Red Ginseng Ethanol Extract Suppressed Ag I/II-induced Up-expression of Inflammatory Mediators in RAW 264.7 Macrophages)

  • 최경민;황승미;임지예;고은실;박종혁;문정혜;이민정;장지은;차정단
    • 한국미생물·생명공학회지
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    • 제43권2호
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    • pp.158-163
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    • 2015
  • 본 연구에서, 우리는 S. mutans Ag I/II 재조합단백질에 의해 유도되어진 염증유발 단백질의 발현에 홍삼 40% 에탄올 추출물의 효과를 알아보고자 하였다. 홍삼에탄올추출물은 Ag I/II 재조합단백질에 의해 유도되어진 염증유발물질들의 mRNA와 단백질의 발현을 억제하였다. 더불어 홍삼에탄올 추출물은 NF-κΒ p65가 핵내로 이용하는 것이 억제하였다. 결론적으로 홍삼 40%에탄올추출물은 NF-κB의 활성에 의해 NO 생성과 iNOS 발현이 조절되어지는 것으로 생각되어지며, 염증유발 관련 유전자들의 낮은 발현을 유도하는 것으로 관찰되어졌다.