• Title/Summary/Keyword: proinflammatory cytokines

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Regulation of RANTES and MCP Expression in Human Nasal Mucosal Fibroblasts (비점막(鼻粘膜) 섬유모세포에서의 RANTES와 MCP의 발현 조절)

  • Ha, Yong-Chan;Cho, Jeong-Je;Yoo, Young-Chun;Yang, Won-Yong
    • IMMUNE NETWORK
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    • v.3 no.1
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    • pp.61-68
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    • 2003
  • Background: Fibroblast functions both as a structural element and as a vital immunoregulatory cell. Fibroblasts regulate inflammation through governing of chemokine expression. In order to elucidate the mechanisms by which the expressions of chemokines were regulated, the co-stimulatory effects of Th1 and proinflammatory cytokines were compared using nasal mucosal fibroblasts. Methods: Human nasal mucosa was obtained from surgery for septal deviation and the growth of fibroblasts was established. Fibroblasts from 4th to 6th passage were stimulated with various combinations of cytokines. To inhibit selected signaling pathways, fibroblasts were pretreated with cyclosporin A, wortmannin, staurosporine, and dexamethasone prior to the stimulation with cytokines. The supernatants were collected and chemokines were detected with a sandwich enzyme-linked immunosorbent assay. Results: $TNF-{\alpha}/IFN-{\gamma}$-induced production of RANTES was inhibited by all inhibitors used. MCP-1 was produced constitutively and $TNF-{\alpha}$-induced or $TNF-{\alpha}/IFN-{\gamma}$-induced production of MCP-1 was not inhibited by cyclosporin A or wortmannin, but by stauroporine or dexamethasone. All inhibitors used in this experiment inhibited $TNF-{\alpha}/IFN-{\gamma}$-induced or $IL-1{\beta}/IFN-{\gamma}$-induced production of MCP-2 in nasal mucosal fibroblasts. Although staurosporine or dexamethasone showed strong inhibitory effects, cyclosporin A or wortmannin did not inhibit the production of MCP-3 by $IL-1{\beta}/IFN-{\gamma}$ treatment. Conclusion: Chemokines were strongly induced by stimulation of cytokines in combination and showed different pattern of inhibition by the inhibitors. Therefore, it was assumed that cytokines acted on multiple pathways or on unknown pathways which converged to gene-specific transcription factors.

Effect of Celeriac Extract on the LPS-Induced Production of Pro-inflammatory Cytokines by RAW 264.7 cells (셀러리악 추출물의 LPS로 유도된 전 염증성 사이토카인 생성에 미치는 영향)

  • Lee, Jae-Hyeok;Jeong, Hyun-Ju;Park, Jeong-Sook
    • Journal of the Korea Convergence Society
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    • v.12 no.2
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    • pp.295-300
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    • 2021
  • This study was conducted to investigate the effect of Celeriac Extract on the production of pro-inflammatory cytokines. Inflammation is caused by pro-inflammatory cytokines TNF-α, IL-6, IL-1β and mediators such as free radicals. We investigated the effect of Celeriac Extract (1ug/mL, 10ug/mL, 100ug/mL) on the production of proinflammatory cytokines such as TNF-α, IL-6, IL-1β and NO by lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. These results demonstrated that Celeriac Extract inhibited the production of TNF-α, IL-6 and NO, without cytotoxicity significantly. Therefore, these findings suggest that Celeriac Extract may attenuate inflammatory responses via inhibition of production of pro-inflammatory cytokines and NO.

Inhibitory Activity of Bumblebee Worker (Bombus terrestris L.) Venoms on Nitric Oxide, TNF-${\alpha}$ and IL-6 Production in Lipopolysaccharide-Activated Macrophages

  • Han Sang-Mi;Lee Kwang-Gill;Yeo Joo-Hong;Kweon Hae-Yong;Woo Soon-Ok;Yoon Hyung-Joo;Baek Ha-Ju;Park Kwan-Kyu
    • International Journal of Industrial Entomology and Biomaterials
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    • v.12 no.2
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    • pp.69-73
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    • 2006
  • To elucidate the composition of bumblebee (Bomb us terrestris) venom (BBV) and the anti-inflammatory effect of BBV. The major components of BBV by LC chromatography and SDS-PAGE were identified. The production of nitric oxide (NO) and proinflammatory cytokines was examined by lipopolysaccharide (LPS) in a macrophage cell line, RAW 264.7 cells, with BBV. BBV inhibits LPS-induced NO in a dose dependent manner. We also found that BBV inhibits proinflammatory cytokine, tumor necrosis factor (TNF)-${\alpha}$ and interleukin (IL)-6 production. These findings mean that BBV can be used in controlling macrophages mediated inflammation related disease. Additional studies on the pharmacological aspects of the individual components of BBV are recommended for future trials.

The Protective Effects of Sasim-tang on the Brain Cell Damage in Photothrombotic Ischemia Mouse Model (광화학적 허혈성 뇌졸중 모델에서 사심탕(瀉心湯)의 뇌세포 손상 보호효과)

  • Kang, Baek-Gyu;Yun, Jong-Min;Moon, Byung-Soon
    • The Journal of Internal Korean Medicine
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    • v.33 no.4
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    • pp.572-586
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    • 2012
  • Objectives : This study was designed to investigate the effects of Sasim-tang (SST) on proinflammatory cytokine production in a photothrombotic ischemia mouse model. Methods : Photothrombotic ischemia was induced in stereotactically held male Balb/c mice using rose bengal (10 mg/kg) and cold light. The target of photothrombotic ischemic lesion was 1 mm anterior to bregma and 3 mm lateral to midline with 2 mm in diameter, which are decreased by oral administration of SST. Results : SST protected ischemic death of brain cells through inhibition of pro-inflammatory cytokines production and catalytic activation of caspase-3 protease in photothrombotic ischemia mouse model. Conclusions : The results of this study suggest that SST can have protective effects on brain cell damage in a photothrombotic ischemia mouse model.

Butein, a tetrahydroxychalcone, suppresses pro-inflammatory responses in HaCaT keratinocytes

  • Seo, Won Yong;Youn, Gi Soo;Choi, Soo Young;Park, Jinseu
    • BMB Reports
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    • v.48 no.9
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    • pp.495-500
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    • 2015
  • Up-regulation of cell adhesion molecules and proinflammatory cytokines contributes to enhanced monocyte adhesiveness and infiltration into the skin, during the pathogenesis of various inflammatory skin diseases, including atopic dermatitis. In this study, we examined the anti-inflammatory effects of butein, a tetrahydroxychalcone, and its action mechanisms using TNF-α-stimulated keratinocytes. Butein significantly inhibited TNF-α-induced ICAM-I expression and monocyte adhesion in human keratinocyte cell line HaCaT. Butein also decreased TNF-α-induced pro-inflammatory mediators, such as IL-6, IP-10 and MCP-1, in HaCaT cells. Butein decreased TNF-α-induced ROS generation in a dose-dependent manner in HaCaT cells. In addition, treatment of HaCaT cells with butein suppressed TNF-α-induced MAPK activation. Furthermore, butein suppressed TNF-α-induced NF-kappaB activation. Overall, our results indicate that butein has immunomodulatory activities by inhibiting expression of proinflammatory mediators in keratinocytes. Therefore, butein may be used as a therapeutic agent for the treatment of inflammatory skin diseases. [BMB Reports 2015; 48(9): 495-500]

MOK, a Pharmacopuncture Medicine, Reduces Inflammatory Response through Inhibiting the Proinflammatory Cytokine Production in LPS-stimulated Mouse Peritoneal Macrophages

  • Hwang, Ji Hye;Hwang, Min Sub;Park, Yong-ki
    • Journal of Acupuncture Research
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    • v.34 no.1
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    • pp.11-21
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    • 2017
  • Objectives : In this study, we investigated the anti-inflammatory and anti-oxidative effects of MOK, a pharmacopuncture medicine, in lipopolysaccharide (LPS)-stimulated mouse peritoneal macrophages. Methods : Peritoneal macrophages were isolated from ICR mice. Primary macrophages were treated with MOK extract (1.25, 2.5, 5, 10, and 20 mg/ml) for 30 min and then stimulated with LPS ($1{\mu}g/ml$) for the indicated times. Cytotoxicity was measured using MTT and LDH assays. Nitric oxide (NO) production in culture supernatants was measured using the Griess assay. The mRNA expression of iNOS, COX-2, proinflammatory cytokines (TNF-${\alpha}$, IL-$1{\beta}$, and IL-6) and antioxidant enzymes (HO-1 and MnSOD) was measured by RT-PCR. Results : Treatment with MOK extract (2.5, 5, and 10 mg/ml) significantly decreased LPS-induced NO production in peritoneal macrophages through inhibition of iNOS expression. The expression of COX-2, TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 mRNA was also decreased in LPS-stimulated macrophages upon treatment with MOK extract. MOK treatment also increased the expression of HO-1 and MnSOD mRNA in macrophages. Conclusion : These results indicate that MOK exerts anti-inflammatory and antioxidant effects by regulating the transcription levels of inflammatory mediators and antioxidant proteins in activated macrophages.

Inhibition of Proinflammatory Cytokine Generation in Lung Inflammation by the Leaves of Perilla frutescens and Its Constituents

  • Lim, Hun Jai;Woo, Kyeong Wan;Lee, Kang Ro;Lee, Sang Kook;Kim, Hyun Pyo
    • Biomolecules & Therapeutics
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    • v.22 no.1
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    • pp.62-67
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    • 2014
  • This study was designed to find some potential natural products and/or constituents inhibiting proinflammatory cytokine generation in lung inflammation, since cytokines such as tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interleukin-6 (IL-6) are pivotal for provoking airway inflammation. In our preliminary screening procedure, the 70% ethanol extract of the leaves of Perilla frutescens (PFE) was found to clearly inhibit TNF-${\alpha}$ production in the lung at 100 mg/kg, after intranasal lipopolysaccharide treatment of mice. Based on this result, ten constituents including phenylpropanoids (allyltetramethoxybenzene, caffeic acid, dillapiole, elemicin, myristicin, nothoapiole, rosmarinic acid methyl ester, rosmarinic acid) and monoterpenes (perilla aldehyde and perilla ketone) were successfully isolated from the extract. Among them, elemicin and myristicin were found for the first time to concentration-dependently inhibit IL-$1{\beta}$-treated IL-6 production from lung alveolar epithelial cells (A549) at concentrations of $10-100{\mu}M$. These findings suggest that the phenylpropanoids including elemicin and myristicin have the potential to be new inhibitory agents against lung inflammation and they may contribute, at least in part, to the inhibitory activity of PFE on the lung inflammatory response.

Senolytics and Senostatics: A Two-Pronged Approach to Target Cellular Senescence for Delaying Aging and Age-Related Diseases

  • Kang, Chanhee
    • Molecules and Cells
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    • v.42 no.12
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    • pp.821-827
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    • 2019
  • Aging is the most important single risk factor for many chronic diseases such as cancer, metabolic syndrome, and neurodegenerative disorders. Targeting aging itself might, therefore, be a better strategy than targeting each chronic disease individually for enhancing human health. Although much should be achieved for completely understanding the biological basis of aging, cellular senescence is now believed to mainly contribute to organismal aging via two independent, yet not mutually exclusive mechanisms: on the one hand, senescence of stem cells leads to exhaustion of stem cells and thus decreases tissue regeneration. On the other hand, senescent cells secrete many proinflammatory cytokines, chemokines, growth factors, and proteases, collectively termed as the senescence-associated secretory phenotype (SASP), which causes chronic inflammation and tissue dysfunction. Much effort has been recently made to therapeutically target detrimental effects of cellular senescence including selectively eliminating senescent cells (senolytics) and modulating a proinflammatory senescent secretome (senostatics). Here, we discuss current progress and limitations in understanding molecular mechanisms of senolytics and senostatics and therapeutic strategies for applying them. Furthermore, we propose how these novel interventions for aging treatment could be improved, based on lessons learned from cancer treatment.

Effects of Sandalwood Essential Oil on the iNOS Expression and Proinflammatory Cytokine Production (Sandalwood Essential Oil의 iNOS 발현과 염증성사이토카인의 생성에 미치는 영향)

  • Park, Jeoung-Suk;Jung, Sook-Heui
    • YAKHAK HOEJI
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    • v.57 no.1
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    • pp.70-75
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    • 2013
  • The present study was designed to determine the effect of the Sandalwood Essential Oil (Santalum album) on pro-inflammatory factors such as NO, iNOS expression and IL-$1{\beta}$, IL-6, TNF-${\alpha}$ in lipopolysaccharide (LPS) - stimulated RAW264.7 macrophages cells. The cell toxicity was determined by MTS assay. To evaluate of anti-inflammatory effect of Sandalwood Essential Oil, amount of NO was measured using the NO detection kit and the iNOS expression was measured by western blot analysis and reverse transcriptase polymerase chain reaction (RT-PCR). And proinflammatory cytokines were measured by ELISA kit. As a result, Sandalwood Essential Oil reduced NO, iNOS expression and IL-$1{\beta}$, IL-6, TNF-${\alpha}$ production without cytotoxicity. Our results suggest that the Sandalwood Essential Oil may have an anti-inflammatory property through suppressing inflammatory mediator productions and appears to be useful as an anti-inflammatory oil.

Antibacterial Activity and Anti-inflammatory Effect of Methanol Extracts of Saliva miltiorrhiza Against Oral Pathogenic Bacteria (단삼 메탄올 추출물의 구강 병원성 세균에 대한 항균 및 항염증효과)

  • Lee, JungHyeok;Yim, Dongsool;Choi, SungSook
    • Korean Journal of Pharmacognosy
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    • v.52 no.1
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    • pp.41-48
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    • 2021
  • This research was conducted to investigate the antibacterial and anti-inflammatory effects of MeOH Ex. of Salvia miltiorrhiza (MESM) against oral pathogenic bacteria. Minimum inhibitory concentration (MIC), removal effect of biofilm produced by Streptococcus mutans, effect of gene expression of proinflammatory cytokines and effect of production of proinflammatory cytokine of MESM were tested. MESM showed moderated antibacterial activity against oral pathogenic bacteria. About 89±8% of biofilms produced by S. mutans were removed by MESM at a concentration of 1 mg/mL. Gene expression of IL-1β and TNF-α induced by Porphyromonas gingivalis were 8~9 folds reduced by MESM. Gene expression of IL-8 induced by Fusobacterium nucelatum were 12 folds reduced by MESM. Production of IL-1β, TNF-α and IL-8 were significantly suppressed by MESM. Conclusively, MESM showed potent antibacterial and anti-inflammatory effect against oral pathogenic bacteria.