• 제목/요약/키워드: proinflammatory mediators

검색결과 129건 처리시간 0.026초

고려인삼에 의한 신경면역 및 염증반응 조절: 백삼사포닌에 의한 교세포에서의 TNF-α, IL-1β 및 NO 생성 증가 (White Ginseng Saponin Upregulated the Production of -TNFTNF-α, IL-1β and NO in Primary Cultures of Mixed Glial Cells)

  • 성정훈;최동희;김동훈;전보권;최상현
    • Journal of Ginseng Research
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    • 제28권2호
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    • pp.120-126
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    • 2004
  • 수천 년 동안 전통적 약제로 사용되어온 고려인삼은 중추신경계의 항상성을 유지하고 면역기능을 강화하는 효능을 나타내는 것으로 알려져 있다. 신경계질환의 진행이 대부분 염증 또는 면역반응을 수반하며, 이로 인하여 손상된 신경세포의 수복과정에 교세포 기원의 매개물질들이 기여하므로, 교세포에서의 cytokine 및 NO생성에 대한 연구는 신경기능과 신경면역기능의 조절 뿐 아니라 신경계 질환에 대한 연구의 초석이라고 할 수 있다. 따라서 본 연구에서는 고려인삼의 신경면역 및 염증반응 조절효과에 대하여 연구하고자 하였으며, 이를 위하여 흰쥐 대뇌피질의 교세포를 일차배양하며 고려인삼사포닌 분획을 처치하여 TNF-$\alpha$, IL-1$\beta$, 및 NO의 생성변동을 연구하였다. 백삼 사포닌은 50-500$\mu\textrm{g}$/ml 용량에서 TNF-$\alpha$와 IL-1$\beta$ 생성을 증가시켰으며, 미세교세포에서 iNOS 발현 및 NO생성을 유도하였고 성상세포의 stellation을 초래하였다. 특히 백삼사포닌 50-100 $\mu\textrm{g}$/ml는 세포독성을 거의 나타내지 않았으므로 이들 용량에 의한 교세포의 적절한 활성화가 중추신경계 면역기능 증가 및 염증반응 조절에 기여할 것으로 생각된다.

두릅순 에탄올 추출물의 인간유래 피부각질형성세포와 피부섬유아세포에서의 자외선에 의한 광노화 억제효과 (Inhibitory effect of Aralia elata ethanol extract against skin damage in UVB-exposed human keratinocytes and human dermal fibroblasts)

  • 양지원;곽충실
    • Journal of Nutrition and Health
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    • 제49권6호
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    • pp.429-436
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    • 2016
  • 본 연구에서는 피부의 표피와 진피에 분포하는 HaCaT 세포와 HDF 세포를 이용하여 항산화효과가 우수한 두릅순 추출물의 처리가 UVB에 의한 피부광노화를 억제할 수 있는지 알아보기 위하여 피부 염증반응과 관련한 사이토카인과 피부의 주요 구성 단백질인 collagen에 영향을 미칠 수 있는 MMP-1, type-I procollagen, TRPV-1 등의 단백질 발현에 미치는 영향을 분석하였다. HaCaT에 두릅순 추출물을 24시간 전처리한 경우 UVB ($55 mJ/cm^2$) 노출로 인해 증가한 염증매개인자인 IL-6, IL-8, $PGE_2$를 유의하게 감소시켰다. 또한, 피부 collagen의 정상적인 구조 및 양에 영향을 미치는 단백질들의 발현을 측정한 결과 HaCaT에서는 UVB 조사로 인해 증가한 TRPV-1과 MMP-1 단백질의 발현이 두릅순 에탄올 추출물의 전처리로 모두 감소하였고, HDF에서는 UVB를 조사한 대조군에 비하여 두릅순 추출물 처리가 MMP-1 단백질 발현을 감소시키는 동시에 collagen의 전구체인 type-I procollagen의 발현을 증가시키는 효과를 보였다. 이들 결과들로부터 항산화효과가 우수한 두릅순 70% 에탄올 추출물은 피부세포에서 UVB에 의한 염증반응을 억제시키는 동시에 피부 collagen의 감소를 억제시킴으로써 피부 광노화를 예방할 수 있는 천연 소재로 이용될 수 있다고 본다.

자화지정 추출물이 LPS로 유발된 대식세포의 염증인자에 미치는 영향 (Effect of Violae Herba Water Extract on the Proinflammatory Factors of LPS-Induced Macrophages)

  • 한효상
    • 디지털융복합연구
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    • 제16권7호
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    • pp.309-316
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    • 2018
  • 본 연구는 지질다당류에 의해 유도된 대식세포주인 RAW 264.7 세포에서 자화지정 추출물이 염증 매개체 생성에 미치는 영향을 조사하고자 하였다. 자화지정 추출물이 대식세포주인 RAW 264.7 세포의 세포 생존 능력에 미치는 영향을 조사 하기 위하여 MTT assay를 실시하였다. 또한, Bio-Plex 사이토카인 분석(cytokine assay)을 통하여 NO, 인터루킨 $(IL)-1{\beta}$, 종양 괴사 인자($TNF-{\alpha}$) 및 IL-6와 같은 다양한 사이토카인(cytokine)의 농도에 의한 자화지정 추출물의 항염증 효과를 조사 하였다. 자화지정 추출물은 LPS로 유도 된 대식세포에서 NO, $IL-1{\beta}$, $TNF-{\alpha}$ 및 IL-6의 농도를 $25{\mu}g/mL$ 이상으로 유의하게 저해하였으며 세포 생존율에는 변화가 없었다. 이러한 결과는 자화지정 추출물이 LPS로 유도된 대식세포에서 $IL-1{\beta}$, $TNF-{\alpha}$ 및 IL-6와 같은 염증성 사이토카인(cytokine)의 억제와 관련된 항염증 효과를 갖는다는 것을 시사한다. 앞으로 자화지정을 이용한 염증질환에 관련된 치료제개발에 새로운 연구가 더 필요한 바이다.

Anthocyanins from Hibiscus syriacus L. Attenuate LPS-Induced Inflammation by Inhibiting the TLR4-Mediated NF-κB Signaling Pathway

  • Karunarathne, Wisurumuni Arachchilage Hasitha Maduranga;Molagoda, Ilandarage Menu Neelaka;Lee, Kyoung Tae;Choi, Yung Hyun;Kang, Chang-Hee;Jeong, Jin-Woo;Kim, Gi-Young
    • 한국자원식물학회:학술대회논문집
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    • 한국자원식물학회 2019년도 추계학술대회
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    • pp.92-92
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    • 2019
  • Excessive or chronic inflammation contributes to the pathogenesis of many inflammatory diseases such as sepsis, rheumatoid arthritis, and ulcerative colitis. Hibiscus syriacus L. has been used as a medicinal plant in many Asian countries, even though its anti-inflammatory activity has been unclear. Therefore, we investigated the anti-inflammatory effect of anthocyanin fractions from the H. syriacus L. varieties Pulsae (PS) on the lipopolysaccharide (LPS)-induced expression of proinflammatory mediators and cytokines in RAW264.7 macrophages. PS suppressed LPS-induced nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) secretion concomitant with downregulation of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. Furthermore, PS inhibited the production of proinflammatory cytokines such as tumor necrosis factor-alpha ($TNF-{\alpha}$), interleukin-6 (IL-6), and IL-12 in LPS-stimulated RAW264.7 macrophages. Further study showed that PS significantly decreased LPS-induced nuclear translocation of the nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) subunits, p65 and p50. Molecular docking data showed that many anthocyanins from PS fit into the hydrophobic pocket of MD2 and bound to Toll-like receptor 4 (TLR4), indicating that PS inhibits the TLR4-MD2-mediated inflammatory signaling pathway. Especially, apigenin-7-O-glucoside most powerfully bound to MD2 and TLR4 through LYS122, LYS122, and SER127 at a distance of $2.205{\AA}$, $3.098{\AA}$, and $2.844{\AA}$ and SER441 at a distance of $2.873{\AA}$ (docking score: -8.4) through hydrogen bonding, respectively. Additionally, PS inhibited LPS-induced TLR4 dimerization/expression on the cell surface, which consequently decreased MyD88 recruitment and IRAK4 phosphorylation. PS completely blocked LPS-mediated mortality in zebrafish larvae by diminishing the recruitment of neutrophil and macrophages accompanied by low levels of proinflammatory cytokines. Taken together, our results indicate that PS attenuates LPS-mediated inflammation in both in vitro and in vivo by blocking the TLR4/MD2-MyD88/IRAK4-$NF-{\kappa}B$ axis. Therefore, PS might be used as a novel modulatory candidate for effective treatment of LPS-mediated inflammatory diseases.

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Involvement of Protein Kinase C-δ in Vascular Permeability in Acute Lung Injury

  • Ahn, Jong J.;Jung, Jong P.;Park, Soon E.;Lee, Minhyun;Kwon, Byungsuk;Cho, Hong R.
    • IMMUNE NETWORK
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    • 제15권4호
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    • pp.206-211
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    • 2015
  • Pulmonary edema is a major cause of mortality due to acute lung injury (ALI). The involvement of protein kinase C-${\delta}$ (PKC-${\delta}$) in ALI has been a controversial topic. Here we investigated PKC-${\delta}$ function in ALI using PKC-${\delta}$ knockout (KO) mice and PKC inhibitors. Our results indicated that although the ability to produce proinflammatory mediators in response to LPS injury in PKC-${\delta}$ KO mice was similar to that of control mice, they showed enhanced recruitment of neutrophils to the lung and more severe pulmonary edema. PKC-${\delta}$ inhibition promoted barrier dysfunction in an endothelial cell layer in vitro, and administration of a PKC-${\delta}$-specific inhibitor significantly increased steady state vascular permeability. A neutrophil transmigration assay indicated that the PKC-${\delta}$ inhibition increased neutrophil transmigration through an endothelial monolayer. This suggests that PKC-${\delta}$ inhibition induces structural changes in endothelial cells, allowing extravasation of proteins and neutrophils.

Effects of the Essential Oil Components from Ligusticum chuanxiong on Proinflammatory Mediators of RAW264.7 Macrophage Cells

  • Lim, Hye-Rim;Shin, Seung-Won
    • Natural Product Sciences
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    • 제16권4호
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    • pp.259-264
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    • 2010
  • The essential oil fraction was obtained from the underground parts o of Ligusticum chuanxiong (Umbelliferae) by steam distillation, and its main components, Z-ligustilide and butylidene phthalide, were isolated by column chromatography. Its essential oil fraction and the isolated main components were examined for effects on their anti-inflammatory properties in RAW 264.7 macrophage cells to develop a new natural anti-inflammatory drug. The results showed that the L. chuanxiong essential oil fraction and its main components, Z-ligustilide and butylidene phthalide, inhibited the production of nitric oxide significantly in lipopolysaccharide (LPS)-treated RAW 264.7 cells. LPS-induced interleukin-$1{\beta}$ (IL-$1{\beta}$), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-$\alpha$) production was also decreased in a dose-dependent manner. In addition, western blot analysis revealed that the L. chuanxiong essential oil fraction and also its main components, Z-ligustilide, and butylidene phthalide reduced the expression levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS).

마우스대식세포주인 RAW 264.7에서 SD-01의 항염증 활성 연구 (Anti-inflammatory effect of SD-01 in RAW 264.7 cells)

  • 박선동
    • 대한본초학회지
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    • 제25권3호
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    • pp.19-25
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    • 2010
  • Objective : The aim of this study was to investigate anti-inflammatory activity of SD-01 methanol extract in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Methods : Cytotoxic activity of SD-01 methanol extract on RAW 264.7 cells was measured using 5-(3-caroboxymeth-oxyphenyl)-2H-tetra-zolium inner salt (MTS) assay. The nitric oxide (NO) production was measured by Griess reagent system. And proinflammatory cytokines and $PGE_2$ were measured by ELISA method. The levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), $I{\kappa}$-B-alpha and nuclear NF-${\kappa}$ B p65 expression were detected by western blot. Results : Our results indicated that methanol extract of SD-01 significantly inhibited the LPS-induced NO, $PGE_2$ production and iNOS, COX-2 expression accompanied by an attenuation of TNF-$\alpha$, IL-$1\beta$, IL-6 and MCP-1 production in RAW 264.7 cells. Moreover, methanol extract of SD-01 treatment also blocked LPS-induced NF-kB activation. Conclusion : These findings indicate that methanol extract of SD-01 inhibits the production of pro-inflammatory mediators and cytokines via suppression of NF-${\kappa}$ B activation. Take together, these results indicate that methanol extract of SD-01 has the potential for use as an agent of anti-chronic inflammatory diseases.

Inhibitory Effects of Jojoongikgi-tang on the Secretion of PGE2 and NO and Cytokines in LPS-stimulated BV2 Microglial Cells

  • Lee, Jun-Moon;Lyu, Sun-Ae;Lee, Seung-Yeon;Kim, Bo-Kyung;Ko, Woo-Shin
    • 대한한방소아과학회지
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    • 제21권2호
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    • pp.97-107
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    • 2007
  • Objectives This experiment is about Jojoongikgi-tang(JIT) exerts anti-inflammatory effects in BV2 microglial cells, and the effect of JIT on Nitric oxide(NO) production in lipopolysaccharide(LPS)-stimulated BV2 microglial cells were also demonstrated. Methods To investigate the anti-inflammatory effects of JIT, NO production, expression level of iNOS mRNA, PGE2 synthesis, expression COX-2 mRNA, cell viability, $TNF-{\alpha}$ mRNA expression were examined. Results The expression level of inducible nitric oxide synthase(iNOS) was decreased by JIT, and the production of Prostaglandin E2(PGE2) and the expression of Cox-2 mRNA also were inhibited by JIT. Proinflammatory mediators, such as $TNF-{\alpha}$, $IL-1{\beta}$, IL-12, were inhibited by JIT in a dose-dependent manner. Conclusions JIT have anti-inflammatory effects in BV2 microglial cells and could be used in inflammatory disease.

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Comparison of Morphine and Tramadol in Transforaminal Epidural Injections for Lumbar Radicular Pain

  • Park, Chan Hong
    • The Korean Journal of Pain
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    • 제26권3호
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    • pp.265-269
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    • 2013
  • Background: Transforaminal epidural steroid injections are known to reduce inflammation by inhibiting synthesis of various proinflammatory mediators and have been used increasingly. The anti-inflammatory properties of opioids are not as fully understood but apparently involve antagonism sensory neuron excitability and pro-inflammatory neuropeptide release. To date, no studies have addressed the efficacy of transforaminal epidural morphine in patients with radicular pain, and none have directly compared morphine with a tramadol for this indication. The aim of this study was to compare morphine and tramadol analgesia when administered via epidural injection to patients with lumbar radicular pain. Methods: A total of 59 patients were randomly allocated to 1 of 2 treatment groups and followed for 3 months after procedure. Each patient was subjected to C-arm guided transforaminal epidural injection (TFEI) of an affected nerve root. As assigned, patients received either morphine sulfate (2.5 mg/2.5 ml) or tramadol (25 mg/0.5 ml) in combination with 0.2% ropivacaine (1 ml). Using numeric rating scale was subsequently rates at 2 weeks and 3 months following injection for comparison with baseline. Results: Both groups had significantly lower mean pain scores at 2 weeks and at 3 months after treatment, but outcomes did not differ significantly between groups. Conclusions: TFEI of an opioid plus local anesthetic proved effective in treating radicular pain. Although morphine surpassed tramadol in pain relief scores, the difference was not statistically significant.

Reconsideration of Classical Antibiotic Lincomycin: Anti-inflammatory Effect in LPS-stimulated RAW 264.7 Cells

  • Yang, Eun-Jin;Lee, Nari;Hyun, Chang-Gu
    • 한국미생물·생명공학회지
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    • 제48권3호
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    • pp.366-372
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    • 2020
  • Since, side effects of antibiotics are frequently emphasized these days, their use is gradually diminishing, and alternative drugs are being developed. We have sought to reintroduce them as raw materials for human health as conventional 'weapons' that have been retired after their historical duties. In this study, we investigated the anti-inflammatory effects of lincomycin (LIN), on lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Our findings show that LIN potently inhibited production of LPS-induced proinflammatory mediators, such as nitric oxide (NO) and prostaglandin E2 (PGE2), without cytotoxicity. Consistent with these findings, LIN strongly decreased protein expression levels of inducible NO synthase (iNOS) and cyclooxygenase (COX-2). Furthermore, LIN reduced pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β. To further elucidate the mechanisms of these inhibitory effects of LIN, we studied LPS-induced IκB-α degradation, and mitogen-activated protein kinase (MAPK) phosphorylation. LIN suppressed downregulation of inhibitory κB (IκB-α) degradation, and the phosphorylation of the c-Jun N-terminal kinase (JNK) pathway. Based on these results, we suggest that LIN may be considered a potential candidate as an anti-inflammatory cosmetic or a medicine for human health.