• Title/Summary/Keyword: proinflammatory cytokine

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β-Sitosterol Contributes in the Resistance to Invasion and Survival of Brucella abortus 544 within RAW264.7 Cells, and Cytokine Production with Reduced Susceptibility to Infection in BALB/c Mice

  • Reyes, Alisha Wehdnesday Bernardo;Arayan, Lauren Togonon;Huy, Tran Xuan Ngoc;Vu, Son Hai;Min, Wongi;Hur, Jin;Kim, Suk
    • Journal of Microbiology and Biotechnology
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    • v.30 no.4
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    • pp.482-489
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    • 2020
  • We previously identified β-sitosterol (BS) as one of the most abundant compounds found in Korean red ginseng oil. BS is a widely prevalent vegetable-derived phytosterol with many known health benefits. Here, we investigated the efficacy of BS against Brucella (B.) abortus infection. BS showed no effect on bacterial growth but attenuated internalization, intracellular survival and MAPKs-linked intracellular signaling in RAW264.7 cells. BS treatment in cells is also associated with increased nitrite concentration during infection at 24 h. Slightly enhanced resistance to B. abortus infection was observed in mice orally given BS, which could be mediated by induced production of proinflammatory cytokines. Taken together, our study demonstrates the contribution of BS treatment against B. abortus infection although further investigation is encouraged to maximize its beneficial effects against intracellular infection.

The Effect of Betulinic Acid on $TNF-{\alpha}-induced$ MCP-1 Expression in HL-60 Cells (HL-60 세포에서 $TNF-{\alpha}$에 의한 MCP-1 발현에 미치는 Betulinic Acid의 효과)

  • Kim, Kyung-Chan;Lee, Chu-Hee
    • YAKHAK HOEJI
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    • v.52 no.1
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    • pp.37-42
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    • 2008
  • Betulinic acid, a naturally occurring pentacyclic triterpenoid, is found in abundance in the outer bark of white birch (Betula alba). In this study, we investigated if betulinic acid affects cytokine expression from activated macrophage cells. ELISA result showed that stimulation of HL-60 cells with proinflammatory cytokine such as $TNF-{\alpha}$ resulted in MCP-1 release into culture medium. In addition, transcriptional upregulation of MCP-1 in response to $TNF-{\alpha}$ was observed by RT-PCR analysis. However, incubation of HL-60 cells with betulinic acid prior to $TNF-{\alpha}$ treatment abrogated MCP-1 expression in transcription and translational level. Consistent with a number of studies which reported requirement of ERK activation for $TNF-{\alpha}$ expression, Western blot analysis showed that $TNF-{\alpha}-induced$ ERK activation was suppressed by pretreatment of HL-60 cells with betulinic acid. Taken together, our data indicate that betulinic acid exerts its anti-inflammatory effect through inhibition of $TNF-{\alpha}-induced$ ERK activation which is required for the subsequent MCP-1 release.

Effects of ChongMyung-Tang and MokguenpiChongMyung-Tang Extract on the Alzheimer's Disease Model Induced by CT105 (총명탕(聰明湯)과 목근피총명탕(木槿皮聰明湯)이 CT105로 유도된 Alzheimer's Disease 병태(病態) 모델에 미치는 영향)

  • Jung, In-Chul;Lee, Sang-Ryong
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.20 no.2
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    • pp.394-403
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    • 2006
  • This research investigated the effect of the CMT and MCMT on Alzheimer's disease. The effects of the CMT and MCMT extract on expression of proinflammatory cytokine($IL-1{\beta}$, IL-6, $TNF-{\alpha}$) in the THP-1 cell; amyloid precursor proteins(APP), acetylcholinesterase(AChE) mRNA of PC-12 cells treated with CT105; the AChE activity and the APP production of PC-12 cell lysate treated with CT105 were investigated. The CMT and MCMT extract suppressed overexpression of $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ in the THP-1 cell treated by LPS; the expression of APP, AChE mRNA in PC-12 cells treated with CT105; the AChE activity and the production of APP in PC-12 cell lysate treated with CT105 significantly. This study suggest that CMT and MCMT may be effective for the prevention and treatment of Alzheimer's disease.

Glial Mechanisms of Neuropathic Pain and Emerging Interventions

  • Jo, Daehyun;Chapman, C. Richard;Light, Alan R.
    • The Korean Journal of Pain
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    • v.22 no.1
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    • pp.1-15
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    • 2009
  • Neuropathic pain is often refractory to intervention because of the complex etiology and an incomplete understanding of the mechanisms behind this type of pain. Glial cells, specifically microglia and astrocytes, are powerful modulators of pain and new targets of drug development for neuropathic pain. Glial activation could be the driving force behind chronic pain, maintaining the noxious signal transmission even after the original injury has healed. Glia express chemokine, purinergic, toll-like, glutaminergic and other receptors that enable them to respond to neural signals, and they can modulate neuronal synaptic function and neuronal excitability. Nerve injury upregulates multiple receptors in spinal microglia and astrocytes. Microglia influence neuronal communication by producing inflammatory products at the synapse, as do astrocytes because they completely encapsulate synapses and are in close contact with neuronal somas through gap junctions. Glia are the main source of inflammatory mediators in the central nervous system. New therapeutic strategies for neuropathic pain are emerging such as targeting the glial cells, novel pharmacologic approaches and gene therapy. Drugs targeting microglia and astrocytes, cytokine production, and neural structures including dorsal root ganglion are now under study, as is gene therapy. Isoform-specific inhibition will minimize the side effects produced by blocking all glia with a general inhibitor. Enhancing the anti-inflammatory cytokines could prove more beneficial than administering proinflammatory cytokine antagonists that block glial activation systemically. Research on therapeutic gene transfer to the central nervous system is underway, although obstacles prevent immediate clinical application.

Metal Effects of Urban Air Particulates on Cytokine Production and DNA Damage

  • Lee, Kwan-Hee;Hong, Yun-Chul
    • Toxicological Research
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    • v.17 no.4
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    • pp.255-265
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    • 2001
  • Epidemiologic studies have demonstrated an association between short-term exposure to particulate air pollutants and increased mortality. However the biological mechanism underlying these associations have not been fully established and also the chemical and physical characteristics of the pollutant particles are not well understood. The metal constituents of air pollutant particles and their bioavailability are considered to Play an important role as possible mediators of Particle-induced airway injury and inflammation. Sprague-Dawley rat alveolar macrophage cells (NR8383) were exposed to airborne and acid-leached particulate matter (PM). Titanium oxide and nickel subsulfide were used as negative and positive controls. Particle-induced reactive oxygen species formation in cells was detected using the fluorescent probe 2',7'-dichlorofluorescin diacetate. Expression of TNF-$\alpha$ and IL-6 were measured by enzyme-linked immunosorbent assay, and PM-induced DNA double-strand breaks were determined with $\lambda$DNA/Hind III marker. Metals associated with air pollutant particles mediated intracellular oxidant production in alveolar macrophages, and the cytotoxicity and proinflammatory cytokine production induced by PM were associated with oxidative stress. The oxidants produced by air pollutant particles also are likely to induce DNA double-strand breaks. Our findings in alveolar macrophage cells exposed to PM and acid-leached PM support the hypothesis that metal components in urban air pollutants and their bioavailabilities might play an Important role in the induction of the adverse health effects.

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Inhibitory effect of epigallocatechin from Camellia sinensis leaves against pro-inflammatory mediator release in macrophages

  • Cho, Jun-Hyo;Hong, Eun-Jin;Cho, Young-Je
    • Journal of Applied Biological Chemistry
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    • v.60 no.3
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    • pp.199-205
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    • 2017
  • To investigate the anti-inflammatory activity of natural products, we determined the anti-inflammatory activity of purified epigallocatechin (EGC) from Camellia sinensis leaves. In the present study, we found that EGC inhibited the production of proinflammatory mediators (IL-6, TNF-${\alpha}$, NO, and $PGE_2$) in lipopolysaccharide (LPS)-stimulated Raw 264.7 cells. Suppression of IL-6 seems to be at least partly attributable to the inhibitory effect of EGC. TNF-${\alpha}$ is a major cytokine produced by LPS-induced macrophages, and they have a wide variety of biological functions including regulation of inflammation. The inhibition of IL-6 and TNF-${\alpha}$ production by EGC may downregulate the acute-phase response to LPS, thereby reducing LPS-induced inflammation. In addition to IL-6 and TNF-${\alpha}$, EGC effectively reduced the production of other key inflammatory mediators, including NO and $PGE_2$. The inhibitory effect of EGC on NO and $PGE_2$ production was supported by the suppression of inducible nitric oxide synthase and COX-2 at protein levels. These results support the traditional use of EGC in the alleviation of various inflammation-associated diseases and suggest that EGC might be useful in the development of new functional foods for inflammatory diseases.

Proinflammatory cytokine levels in oral lichen planus, oral leukoplakia, and oral submucous fibrosis

  • Kaur, Jasdeep;Jacobs, Reinhilde
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.41 no.4
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    • pp.171-175
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    • 2015
  • Objectives: The objective of this study was to identify salivary and serum concentrations of interleukin (IL)-8, IL-6, and tumor necrosis factor alpha ($TNF-{\alpha}$) in patients with oral lichen planus, oral leukoplakia, oral submucous fibrosis, and healthy controls. Materials and Methods: Patients selected included 54 oral lichen planus (41 to 65 years), 50 oral leukoplakia (42 to 65 years), 51 oral submucous fibrosis (41 to 65 years), and 50 healthy controls (42 to 65 years). Oral lichen planus, oral leukoplakia, and oral submucous fibrosis cases were diagnosed using histopathological analysis. Salivary and serum cytokine concentrations were measured using enzyme-linked immunoassay kits in all subjects. Results: The levels of serum and salivary $TNF-{\alpha}$, IL-6, and IL-8 were statistically significantly increased in oral leukoplakia, submucous fibrosis, and lichen planus in contrast to normal healthy subjects (P<0.05). Serum and salivary correlation analysis revealed strong and highly significant correlations for $TNF-{\alpha}$, IL-6, and IL-8 in all groups (r=0.72-0.82, P<0.05). Conclusion: Salivary and serum cytokines were also elevated when analyzed in oral precancerous lesions. Thus, salivary and serum IL-8, IL-6, and TNF-${\alpha}$ levels might act as diagnostic markers for detection of oral precancer.

Inhibitory Effect of Brassica rapa in Ovalbumin-Stimulated Experimental Asthmic Mice

  • Bae, Eun-Ah;Min, Seung-Won;Kim, Nam-Jae;Bang, Myung-Ho;Baek, Nam-In;Han, Eun-Joo;Chung, Hae-Gon;Kim, Dong-Hyun
    • Natural Product Sciences
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    • v.13 no.2
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    • pp.114-117
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    • 2007
  • To evaluate antiallergic effect of Brassica rapa Metzg (BR, Family Cruciferae), which is widely used as a food source, its anti-asthmic effect was investigated. BR reduced IgE level in the blood of ovalbumin (OVA)-induced asthmic mice. BR also inhibited IgE and ploinflammatory cytokine IL-6 productions in trachea of OVA-induced mice, but did not inhibit IL-4 production. BR did not inhibit mRNA expression of proinflammatory cytokines IL-6 and IL-4 in IgE-induced RBL-2H3 cells. BR and its isolated components 10-undecenoic acid 2-methoxy methyl ester and galactosyl diglyceride potently inhibited the NO production of RAW264.7cells induced by lipopolysaccharide. These findings suggest that the anti-asthmic effect of BR may be due to the inhibition of the biosynthesis of proinflarnmatory cytokine IL-6 in macrophage and BR can improve IgE-induced allergic disease asthma.

Effects of ChongMyung-Tang and SansaChongMyung-Tang Extract on the Alzheimer's Disease Model Induced dy CT105 (총명탕(聰明湯)과 산사총명탕(山査聰明湯)이 CT105로 유도된 Alzheimer's Disease 병태 모델에 미치는 영향)

  • Lee Sang-Ryong;Jung In-Chul
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.20 no.1
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    • pp.138-148
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    • 2006
  • This research investigated the effect of the CMT and SCMT on Alzheimer's disease. The effects of the CMT and SCMT extract on expression of proinflammatory cytokine(IL-$1{\beta}$, IL-6, TNF-$\alpha$) in the THP-1 cell; amyloid precursor proteins(APP), acetylcholinesterase(AChE) mRNA of PC-12 cells treated with CT105; the AChE activity and the APP production of PC-12 cell lysate treated with CT105 were investigated. The CMT and SCMT extract suppressed overexpression of IL-$1{\beta}$, IL-6, TNF-$\alpha$ in the THP-1 cell treated dy LPS; the expression of APP, AChE mRNA in PC-12 cells treated with CT105; the AChE activity and the production of APP in PC-12 cell Iysate treated with CT105 significantly. This study suggest that CMT and SCMT may be effective for the prevention and treatment of Alzheimer's disease.

Anti-inflammatory Effect of Angelicae acutilobae Radix Water Extract on LPS-stimulated Mouse Macrophages (마우스 대식세포를 이용한 일당귀 물추출물의 항염효능 연구)

  • Han, Hyo-Sang
    • The Korea Journal of Herbology
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    • v.28 no.6
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    • pp.129-133
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    • 2013
  • Objectives : The purpose of this study was to investigate the effects of Angelicae acutilobae Radix Water Extract (AA) on the production of cytokines in RAW 264.7 cell stimulated with lipopolysaccharide (LPS). Method : RAW 264.7 cells were cotreated with AA (50 and $100{\mu}g/mL$) and lipopolysaccharide (LPS; $1{\mu}g/mL$) for 24 hours. After 24 hours treatment, using bead-based multiplex cytokine assay, concentrations of various cytokines such as interleukin(IL)-6, tumor necrosis factor-alpha(TNF-${\alpha}$) granulocyte colony-stimulating factor(G-CSF), granulocyte macrophage colony-stimulating factor(GM-CSF), and macrophage inflammatory protein(MIP)-$1{\alpha}$ were measured. Result : AA significantly inhibited LPS-induced production of IL-6 and MIP-$1{\alpha}$ from LPS-stimulated RAW 264.7 cells at the concentration of $50{\mu}g/mL$. AA significantly inhibited LPS-induced production of TNF-${\alpha}$ from LPS-stimulated RAW 264.7 cells at the concentration of $100{\mu}g/mL$. AA significantly inhibited LPS-induced production of G-CSF and GM-CSF in RAW 264.7 cells at the concentrations of 50 and $100{\mu}g/mL$. Conclusion : These results suggest that AA has anti-inflammatory effect related with its inhibition of proinflammatory cytokines such as IL-6, TNF-${\alpha}$, G-CSF, GM-CSF, and MIP-$1{\alpha}$ in LPS-induced macrophages.