• 제목/요약/키워드: tumor necrosis factor-{\alpha}

검색결과 1,702건 처리시간 0.028초

The Effects of Danchunwhangagam on LPS or DFX-induced Cytokine Production in Peripheral Mononuclear Cells of Cerebral Infarction Patients

  • Son, Ji-Young;Lee, Key-Sang
    • 대한한의학회지
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    • 제26권4호
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    • pp.1-11
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    • 2005
  • This study was to investigate the effect of Danchunwhangagam(DCWGG) extract on the production of proinflammatory cytokines in peripheral blood mononuclear cells (PBMCs) from Cerebral infarction(CI) patients. Methods: We examined how the inhibition rate of tumor necrosis factor (TNF)-$\alpha$, interleukin(IL)-1$\alpha$, IL-1$\beta$, IL-6, and IL-8 productions in DCWGG pretreatment PBMCs culture supernatant in the lipopolysaccaride(LPS)- or desferrioxamine(DFX)treated cells compared to unstimulated cells. Results: DCWGG inhibited the productions of TNF-$\alpha$, IL-1$\alpha$, IL-1$\beta$, IL-6, and IL-8 induced by LPS in a dose-dependent manner. Conclusions: DCWGG might have regulatory effects on LPS or DFX-induced cytokine production, which might explain its beneficial effect in the treatment of CI.

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단천환가감이 중풍 환자의 말초 단핵구에서 LPS 및 DFX 유도성 사이토카인 생성에 미치는 영향 (Effects of Danchunwhangagam on LPS or DFX-induced Cytokine Production in Peripheral Mononuclear Cells of Cerebral Infarction Patients)

  • 이성근;이기상
    • 동의생리병리학회지
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    • 제20권4호
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    • pp.929-935
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    • 2006
  • This study was to investigate the effect of Danchunwhangagam(DCWGG) extract on the production of proinflammatory cytokines in peripheral mononuclear cells (PBMCS) from Cerebral infarction(CI) patients. Methods: We examined that the inhibition rate of tumor necrosis factor $(TNF)-{\alpha},\;interleukin(IL)-1{\alpha},\;IL-1{\beta}$, IL-6, and IL-8 productions in DCWGG pretreatment PBMCs culture supernatant in the lipopolysaccaride(LPS)- or Oesferrioxamine(DFX)-treated cells compared to unstimulated cells. DCWGG inhibited the productions of $TNF-{\alpha},\;IL-1{\alpha},\;IL-1{\beta}$, IL-6, and IL-8 induced by LPS in a dose-dependent manner DCWGG might have regulatory effects on LPS or DFX-induced cytokine production, which might explain its beneficial effect in the treatment of CI.

파슬리추출물의 피부 노화 방지와 자극 완화에 대한 효과 (Effects of Parsley Extract on Skin Anti-aging and Anti-irritation)

  • 김수남;이소희;최규호;장이섭;이병곤
    • 대한화장품학회지
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    • 제30권1호
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    • pp.79-83
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    • 2004
  • 파슬리추출물이 피부에 미치는 개선효과를 조사하기 위하여, 배양 인체 섬유아세포에서 total Collagen, type I procollagen을 각질형성세포주인 HaCaT 세포에서 prostaglandin E$_2$(PGE$_2$), interleukin l$\alpha$ (IL-l$\alpha$)와 tumor necrosis factor $\alpha$ (TNF$\alpha$)를 무모생쥐(Female albino hairless mice, Skh:hr-1)에서는 진피의 두께와 밀도를 측정하였다. 그 결과, 1 $\mu\textrm{g}$/mL 농도의 파슬리 추출물은 total collagen은 23%, type I procollagen은 18% 증가시켰고, 자외선 B에 의한 PGE$_2$의 생합성은 약 60% 정도 감소시켰다. 10uM RA, 100 $\mu\textrm{g}$/mL SLS와 자외선 B 30 mJ/$\textrm{cm}^2$로 조사했을 때, IL-1$\alpha$ 및 TNF $\alpha$의 생합성 역시 1 $\mu\textrm{g}$/mL 파슬리추출물 처리 시 감소되었다. 4일 동안 1% 파슬리추출물로 폐쇄첩포한 무모생쥐의 진피 두께는 대조군에 비해 약 1.5배 정도 두꺼워지고, 밀도도 훨씬 촘촘해졌다. 본 연구의 결과는 파슬리추출물이 피부에서 노화방지 효과 및 자극완화 효과가 있음을 시사하고 있다.

The Anti-Inflammatory Effects of Phytochemicals by the Modulation of Innate Immunity

  • Youn, Hyung-Sun
    • 대한의생명과학회지
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    • 제18권3호
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    • pp.181-192
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    • 2012
  • Toll-like receptors (TLRs) induce innate immune responses that are essential for host defense against invading microbial pathogens. In general, TLRs have two major downstream signaling pathways; myeloid differential factor 88 (MyD88) and Toll/IL-1R domain-containing adaptor inducing IFN-${\beta}$ (TRIF) leading to the activation of NF-${\kappa}B$ and IRF3. Numerous studies demonstrated that certain phytochemicals possessing anti-inflammatory effects inhibit NF-${\kappa}B$ activation induced by pro-inflammatory stimuli including lipopolysaccharide and tumor necrosis factor-${\alpha}$ ($TNF{\alpha}$). However, the direct molecular targets for such anti-inflammatory phytochemicals are not fully identified. In this paper, we will discuss about the molecular targets of phytochemicals in TLRs signaling pathways. These results present a novel anti-inflammatory mechanism of phytochemicals in TLRs signaling.

Protein tyrosine phosphatase PTPN21 acts as a negative regulator of ICAM-1 by dephosphorylating IKKβ in TNF-α-stimulated human keratinocytes

  • Cho, Young-Chang;Kim, Ba Reum;Cho, Sayeon
    • BMB Reports
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    • 제50권11호
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    • pp.584-589
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    • 2017
  • Intercellular adhesion molecule-1 (ICAM-1), which is induced by tumor necrosis factor (TNF)-${\alpha}$, contributes to the entry of immune cells into the site of inflammation in the skin. Here, we show that protein tyrosine phosphatase non-receptor type 21 (PTPN21) negatively regulates ICAM-1 expression in human keratinocytes. PTPN21 expression was transiently induced after stimulation with TNF-${\alpha}$. When overexpressed, PTPN21 inhibited the expression of ICAM-1 in HaCaT cells but PTPN21 C1108S, a phosphatase activity-inactive mutant, failed to inhibit ICAM-1 expression. Nuclear factor-${\kappa}B$ (NF-${\kappa}B$), a key transcription factor of ICAM-1 gene expression, was inhibited by PTPN21, but not by PTPN21 C1108S. PTPN21 directly dephosphorylated phospho-inhibitor of ${\kappa}B$ ($I{\kappa}B$)-kinase ${\beta}$ ($IKK{\beta}$) at Ser177/181. This dephosphorylation led to the stabilization of $I{\kappa}B{\alpha}$ and inhibition of NF-${\kappa}B$ activity. Taken together, our results suggest that PTPN21 could be a valuable molecular target for regulation of inflammation in the skin by dephosphorylating p-$IKK{\beta}$ and inhibiting NF-${\kappa}B$ signaling.

TSG101 Physically Interacts with Linear Ubiquitin Chain Assembly Complex (LUBAC) and Upregulates the TNFα-Induced NF-κB Activation

  • Eunju Kim;Hyunchu Cho;Gaeul Lee;Heawon Baek;In Young Lee;Eui-Ju Choi
    • Molecules and Cells
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    • 제46권7호
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    • pp.430-440
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    • 2023
  • Linear ubiquitin chain assembly complex (LUBAC) is a ubiquitin E3 ligase complex composed of HOIP, HOIL-1L, and SHARPIN that catalyzes the formation of linear/M1-linked ubiquitin chain. It has been shown to play a pivotal role in the nuclear factor (NF)-κB signaling induced by proinflammatory stimuli. Here, we found that tumor susceptibility gene (TSG101) physically interacts with HOIP, a catalytic component of LUBAC, and potentiates LUBAC activity. Depletion of TSG101 expression by RNA interference decreased TNFα-induced linear ubiquitination and the formation of TNFα receptor 1 signaling complex (TNF-RSC). Furthermore, TSG101 facilitated the TNFα-induced stimulation of the NF-κB pathway. Thus, we suggest that TSG101 functions as a positive modulator of HOIP that mediates TNFα-induced NF-κB signaling pathway.

Lipopolysaccharide로 유발된 마우스 대식세포의 염증매개성 Cytokine 생성증가에 대한 참당귀 물추출물의 효능 연구 (Anti-inflammatory Effect of Angelicae Gigantis Radix Water Extract on LPS-stimulated Mouse Macrophages)

  • 한효상
    • 대한본초학회지
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    • 제28권5호
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    • pp.113-119
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    • 2013
  • Objectives : The purpose of this study was to investigate the effects of Angelicae Gigantis Radix Water Extract(AG) on the production of proinflammatory mediators in RAW 264.7 cells stimulated with lipopolysaccharide(LPS). Method : RAW 264.7 cells were cotreated with AG(50 and 100 ug/mL) and lipopolysaccharide(LPS; 1 ug/mL) for 24 hours. After 24 hour treatment, using Bead-based multiplex cytokine assay, concentrations of various cytokines such as interleukin(IL)-6, IL-$1{\beta}$, IL-10, tumor necrosis factor-alpha(TNF-${\alpha}$), granulocyte colony-stimulating factor(G-CSF), granulocyte macrophage colony-stimulating factor(GM-CSF), interferon inducible protein-10(IP-10), leukemia inhibitory factor(LIF), lipopolysaccharide-induced chemokine(LIX), monocyte chemoattractant protein-1(MCP-1), macrophage colony-stimulating factor(M-CSF), macrophage inflammatory protein(MIP)-$1{\alpha}$, MIP-$1{\beta}$, MIP-2, Regulated on Activation, Normal T cell Expressed and Secreted(RANTES) and vascular endothelial growth factor(VEGF) were measured. Result : AG significantly inhibited LPS-induced production of TNF-${\alpha}$, MIP-$1{\alpha}$, G-CSF, RANTES, IL-10, and M-CSF from LPS-stimulated RAW 264.7 cells at the concentrations of 50 and 100 ug/mL. AG significantly inhibited LPS-induced production of MIP-$1{\beta}$, MIP-2, GM-CSF, and IL-6 from LPS-stimulated RAW 264.7 cells at the concentrations of 50 ug/mL. AG significantly inhibited LPS-induced production of VEGF from LPS-stimulated RAW 264.7 cells at the concentrations of 100 ug/mL. But AG did not show any significant effect on the production of MCP-1, LIF, LIX, IP-10 and IL-$1{\beta}$ from LPS-induced RAW 264.7 cells. Conclusion : These results suggest that AG has anti-inflammatory effect related with its inhibition of proinflammatory mediators such as TNF-${\alpha}$, MIP-$1{\alpha}$, G-CSF, RANTES, IL-10, MIP-$1{\beta}$, MIP-2, GM-CSF, IL-6, VEGF and M-CSF in LPS-induced macrophages.

The mechanism of human neural stem cell secretomes improves neuropathic pain and locomotor function in spinal cord injury rat models: through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities

  • I Nyoman Semita;Dwikora Novembri Utomo;Heri Suroto;I Ketut Sudiana;Parama Gandi
    • The Korean Journal of Pain
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    • 제36권1호
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    • pp.72-83
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    • 2023
  • Background: Globally, spinal cord injury (SCI) results in a big burden, including 90% suffering permanent disability, and 60%-69% experiencing neuropathic pain. The main causes are oxidative stress, inflammation, and degeneration. The efficacy of the stem cell secretome is promising, but the role of human neural stem cell (HNSC)-secretome in neuropathic pain is unclear. This study evaluated how the mechanism of HNSC-secretome improves neuropathic pain and locomotor function in SCI rat models through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities. Methods: A proper experimental study investigated 15 Rattus norvegicus divided into normal, control, and treatment groups (30 µL HNSC-secretome, intrathecal in the level of T10, three days post-traumatic SCI). Twenty-eight days post-injury, specimens were collected, and matrix metalloproteinase (MMP)-9, F2-Isoprostanes, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, and brain derived neurotrophic factor (BDNF) were analyzed. Locomotor recovery was evaluated via Basso, Beattie, and Bresnahan scores. Neuropathic pain was evaluated using the Rat Grimace Scale. Results: The HNSC-secretome could improve locomotor recovery and neuropathic pain, decrease F2-Isoprostane (antioxidant), decrease MMP-9 and TNF-α (anti-inflammatory), as well as modulate TGF-β and BDNF (neurotrophic factor). Moreover, HNSC-secretomes maintain the extracellular matrix of SCI by reducing the matrix degradation effect of MMP-9 and increasing the collagen formation effect of TGF-β as a resistor of glial scar formation. Conclusions: The present study demonstrated the mechanism of HNSC-secretome in improving neuropathic pain and locomotor function in SCI through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities.

Lipopolysaccharide (LPS)에 의해 유도된 염증에 대한 건조 고등어 추출물의 항염증 효과 (Protective Effect of Dried Mackerel Extract on Lipopolysaccharide-induced Inflammation)

  • 김광혁;최명원;최향미;임선영
    • 생명과학회지
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    • 제23권9호
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    • pp.1140-1146
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    • 2013
  • 본 연구에서는 건조 고등어 추출물 및 분획물들에 의한 nitric oxide 생성에 미치는 영향을 살펴보았고 건조 고등어 85% aq. MeOH 분획물을 중심으로 면역과정의 생물학적 작용과 대사적 변화를 유도하는 IL-6, IFN-${\gamma}$ 및 TNF-${\alpha}$ 같은 pro-inflammatory 사이토카인의 생성을 측정하여 건조 고등어 추출물에 의한 항염증 효과에 대하여 검토하였다. 건조 고등어 추출물과 각 분획물은 control보다 낮은 nitric oxide 생성량을 나타내었으며, 특히 85% aq. MeOH 및 n-hexane 분획물에 의한 저해효과가 높았다. 건조 고등어 분획물은 Con-A 보다는 LPS에 의해 자극된 IL-6, TNF-${\alpha}$ 및 IFN-${\gamma}$의 생성을 감소시키는데 더 효과적이었다. IL-6 및 TNF-${\alpha}$의 생성은 배양시간 6시간 후 건조 고등어 85% aq. MeOH 분획물의 모든 첨가농도(1, 3 및 $10{\mu}g$)에서 감소되었다(p<0.05). IFN-${\gamma}$의 경우, 건조 고등어 85% aq. MeOH 분획물을 LPS와 함께 처리했을 때 특히 72시간 배양 시 IFN-${\gamma}$의 생성량이 농도 의존적으로 감소하였고 Con-A에 의해 자극된 IFN-${\gamma}$의 생성량은 6 및 24시간 배양 후 유의적으로 감소하였다(p<0.05). 이상의 결과로부터 건조 고등어 85% aq. MeOH 분획물은 nitric oxide 생성과 pro-inflammatory 사이토카인(IL-6, TNF-${\alpha}$, and IFN-${\gamma}$)을 감소시켜 염증반응을 예방할 것으로 기대된다.

Tumor Necrosis Factor-α Gene Polymorphisms and Risk of Oral Cancer: Evidence from a Meta-analysis

  • Chen, Fang-Chun;Zhang, Fan;Zhang, Zhi-Jiao;Meng, Si-Ying;Wang, Yang;Xiang, Xue-Rong;Wang, Chun;Tang, Yu-Ying
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권12호
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    • pp.7243-7249
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    • 2013
  • Numerous studies have been conducted regarding association between TNF-${\alpha}$ and oral cancer risk, but the results remain controversial. The present meta-analysis is performed to acquire a more precise estimation of relationships. Databases of Pubmed, the Cochrane library and the China National Knowledge Internet (CNKI) were retrieved until August 10, 2013. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated with fixed- or random-effect models. The heterogeneity assumption was assessed by I-squared test. Among the eight included case-control studies, all were focused on TNF-${\alpha}$-308G>A and four also concerned the TNF-${\alpha}$-238G>A polymorphism. It was found that oral cancer risk were significant decreased with the TNF-${\alpha}$-308G>A polymorphism in the additive genetic model (GG vs. AA, OR=0.19, 95% CI: [0.04, 1.00], P=0.05, I2=68.9%) and the dominant genetic model (GG+GA vs. AA, OR=0.22, 95% CI: [0.06, 0.82], P=0.03, I2=52.4%); however, no significant association was observed in allele contrast (G vs. A, OR=0.70, 95% CI: [0.23, 2.16], P=0.54, I2=95.9%) and recessive genetic models (GG vs. GA+AA, OR=0.72, 95% CI: [0.33, 1.57], P=0.41, I2=93.1%). For the TNF-${\alpha}$-238G>A polymorphism, significant associations with oral cancer risk were found in the allele contrast (G vs. A, OR=2.75, 95% CI: [1.25, 6.04], P=0.01, I2=0.0%) and recessive genetic models (GG vs. GA+AA, OR=2.23, 95%CI: [1.18, 4.23], P=0.01, I2=0.0%). Conclusively, this meta-analysis indicates that TNF-${\alpha}$ polymorphisms may contribute to the risk of oral cancer. Allele G and the GG+GA genotype of TNF-${\alpha}$-308G>A may decrease the risk of oral cancer, while allele G and the GG genotype of TNF-${\alpha}$-238G>A may cause an increase.