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Gyo-Jeong Gu Sang-Il Ahn Se Jin Lim Ji Hun Paek Songmun Kim Soon Sung Lim Hyung-Sun Youn 《Food science and biotechnology》2014,23(2):587-592
Inflammation can be mediated by invading microbial pathogens. Toll-like receptors (TLRs) recognize invading microbial pathogens, inducing innate immune responses. Broadly, the activation of TLRs induces two major downstream signaling pathways, myeloid differential factor 88 (MyD88)- and Toll/interleukin 1 receptor domain-containing adapter inducing interferon-β (TRIF)-dependent pathways, which lead to the activation of nuclear factor-κB (NF-κB) and interferon regulatory factor 3 (IRF3). To evaluate the therapeutic potential of the ethanol extracts of flowers of Eupatorium japonicum Thunb (EJE), its effect on signal transduction via the TLR signaling pathways induced by lipopolysaccharide (LPS) or polyinosinic-polycytidylic acid (poly[I:C]) was examined. EJE suppressed the activation of NF-κB and IRF3 induced by LPS or poly[I:C]. EJE also inhibited LPS- or poly[I:C]-induced IRF3 phosphorylation as well as interferon-inducible genes, such as interferon inducible protein-10. These results suggest that EJE can modulate TLR signaling pathways, realizing effective therapeutic options for chronic inflammatory diseases. 相似文献
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Gyo-Jeong Gu Sang-Hoon Eom Hwa-Jeong Shin Ji Hun Paek Songmun Kim Soon Sung Lim Hyung-Sun Youn 《Food science and biotechnology》2013,22(3):811-815
Toll-like receptors (TLR) play an important role in the recognition of many pathogen-associated molecular patterns and the induction of innate immunity. Dysregulated activation of TLR signaling pathways is associated with certain inflammatory diseases. Japanese bog orchid (Eupatorium japonicum), which belongs to a family of Asteraceae plants, is consumed as a tea. The present study investigated the effect of the ethanol extracts of flowers of Japanese bog orchid (EJE) on nuclear factor (NF)-κB activation and expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) by TLR agonists in murine macrophages. EJE suppressed NF-κB activation and iNOS and COX-2 expression induced by lipopolysaccharide (TLR4 agonist), polyriboinosinic polyribocytidylic acid (TLR3), and macrophage-activating 2 kDa lipopeptide (TLR2 and TLR6). These results suggest that EJE can regulate TLR signaling pathways and indicated its potential as a potent anti-inflammatory drug. 相似文献
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Abdelali Daddaoua Enrique Martínez-Plata Mercedes Ortega-González Borja Ocón Carlos J. Aranda Antonio Zarzuelo María D. Suárez Fermín Sánchez de Medina Olga Martínez-Augustin 《Food chemistry》2013,136(3-4):1288-1295
Active Hexose Correlated Compound (AHCC) is an immunostimulatory nutritional supplement. AHCC effects and mechanism of action on intestinal epithelial cells or monocytes are poorly described. AHCC was added to the culture medium of intestinal epithelial cells (IEC18 and HT29 cells) and monocytes (THP-1 cells) and assessed the secretion of proinflammatory cytokines by ELISA. Inhibitors of NFκB and MAPKs were used to study signal transduction pathways while TLR4 and MyD88 were silenced in IEC18 cells using shRNA. It was found that AHCC induced GROα and MCP1 secretion in IEC18 and IL-8 in HT29 cells. These effects depended on NFκB activation, and partly on MAPKs activation and on the presence of MyD88 and TLR4. In THP-1 cells AHCC evoked IL-8, IL-1β and TNF-α secretion. The induction of IL-8 depended on JNK and NFκB activation. Therefore, AHCC exerts immunostimulatory effects on intestinal epithelial cells and monocytes involving TLR4/MyD88 and NFκB/MAPK signal transduction pathways. 相似文献
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目的:基于TLR4/NF-κB信号通路探讨黔产刺梨根治疗溃疡性结肠炎大鼠的作用机制。方法:采用2,4,6-三硝基苯磺酸(TNBS)/乙醇溶液灌肠建立溃疡性结肠炎模型,灌胃刺梨根水煎液高、中、低剂量组(8、4、2 g/kg),柳氮磺嘧啶组(0.3 g/kg)。观察大鼠外观、动作行为以及血便;采集大鼠血清与大鼠结肠,利用苏木素-伊红(HE)染色观察各组大鼠结肠病理学改变;酶联免疫吸附测定(ELISA)检测大鼠血清白细胞介素(IL)-1β,IL-6,TNF-α水平;逆转录聚合酶链式反应(RT-PCR)检测大鼠结肠Myd88、NF-κB p50、NF-κB p65、TLR4 mRNA表达;蛋白免疫印迹法(Western blot)检测大鼠结肠Myd88、NF-κB p50、NF-κB p65、TLR4蛋白表达。结果:刺梨根水煎液可明显改善溃疡性结肠炎大鼠结肠炎症损伤,特别是刺梨根水煎液高剂量组。与模型组比较,刺梨根水煎液高剂量组结肠病理损伤得到显著改善,刺梨根水煎液高剂量组血清IL-1β、IL-6、TNF-α水平均极显著下降(P<0.01);结肠Myd88、NF-κB p50、TLR4 mRNA表达量显著下降(P<0.05);结肠Myd88、NF-κB p50、NF-κB p65、TLR4蛋白表达量极显著下降(P<0.01)。结论:刺梨根水煎液可有效缓解TNBS诱导的溃疡性结肠炎并改善炎症损伤,刺梨根水煎液干预溃疡性结肠炎的作用机制可能与抑制TLR4/NF-κB信号通路相关。 相似文献
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目的:探讨榆干离褶伞溶栓酶对脂多糖(lipopolysaccharide,LPS)诱导的血管内皮细胞炎性损伤的保护作用。方法:以LPS诱导人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVEC)炎性损伤。将HUVEC分为空白对照组、模型组和榆干离褶伞溶栓酶(Lyophyllum ulmarium fibrinolytic enzyme,LUFE)低、中、高剂量组。采用噻唑蓝法测定HUVEC存活率,通过酶联免疫吸附测试法检测细胞上清液乳酸脱氢酶(lactate dehydrogenase,LDH)、肿瘤坏死因子α(tumor necrosis factor α,TNF-α)、白介素6(interleukin 6,IL-6)、E-选择素和单核细胞趋化因子1(monocyte chemoattractant protein 1,MCP-1)水平。流式细胞术检测细胞间黏附分子1(intercellular cell adhesion molecule 1,ICAM-1)表达水平,采用Hoechst染色法观察HUVEC与人急性单核细胞白血病细胞系(human acute monocytic leukemia cell line-1,THP-1)的黏附作用。用蛋白印迹实验检测HUVEC的Toll样受体4(toll-like receptor 4,TLR4)、丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)以及核因子-κB(nuclear factor κB,NF-κB)通路中主要蛋白(髓样分化因子88(myeloid differentiation factor 88,MyD88)、转化生长因子β激活激酶1(transforming growth factor β activated kinase 1,TAK1)、磷酸化TAK1(phosphorylated TAK1,p-TAK1))的表达和活化情况。结果:LUFE能够抑制LPS所诱导的HUVEC培养上清液LDH、TNF-α、IL-6、E-选择素和MCP-1水平的升高,降低细胞ICAM-1表达水平并减弱HUVEC与THP-1的黏附作用。与模型组比较,LUFE各剂量组TLR4、MyD88、p-TAK1/TAK1、磷酸化c-Jun氨基末端激酶(phosphorylated c-Jun N-terminal kinase,p-JNK)/JNK、p-p38/p38、p-NF-κB/NF-κB水平显著降低(P<0.05)。结论:LUFE对血管内皮细胞的炎性损伤具有保护作用,其作用机制可能是通过抑制TLR4/MyD88/TAK1/NF-κB信号通路及MAPK通路,进而降低炎症因子水平,从而保护血管内皮细胞。 相似文献
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目的:探究牛蒡子苷元(arctigenin,ATG)对于糖尿病小鼠肝损伤的保护作用。方法:通过四氧嘧啶诱导雄性ICR小鼠建立糖尿病模型,设置对照组、模型组、阳性二甲双胍(metformin,Met)组以及ATG高、中、低剂量组(120、90、60 mg/kg mb),测定小鼠血清中谷丙转氨酶(alanine aminotransferase,ALT)和谷草转氨酶(asparate aminotransferase,AST)活力以及炎症因子白细胞介素-6(interleukin-6,IL-6)和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)质量浓度;分析肝脏内谷胱甘肽(glutathione,GSH)、过氧化氢酶(catalase,CAT)和超氧化物歧化酶(superoxide dismutase,SOD)水平;对比肝脏染色切片组织形态、组织Toll样受体4(toll-like receptors 4,TLR4)、髓样分化因子88(myeloid differentiation factor 88,MyD88)、核因子κB p65(nuclear factor κB p65,NF-κB p65)信号通路中相关蛋白表达情况。结果:与模型组相比,ATG高剂量干预极显著降低了糖尿病小鼠血清中ALT活力和AST活力(P<0.01);ATG高、中剂量极显著降低了炎症因子IL-6、TNF-α质量浓度(P<0.01);ATG高剂量极显著提高了糖尿病小鼠肝脏内CAT、SOD活力(P<0.01),显著提高GSH含量(P<0.05);ATG高、中剂量明显改善了肝脏组织细胞形态,使苏木精-伊红染色切片中细胞内染红面积增大,细胞空泡和出血区域减少;ATG高剂量显著降低了肝脏内TLR4、MyD88和NF-κB p65蛋白表达量(P<0.05、P<0.01)。ATG保护糖尿病肝损伤作用机理可能是通过降低TLR4、MyD88、NF-κB p65炎性通路中关键蛋白的表达水平,抑制下游的TNF-α、IL-6等炎症因子表达,进而降低氧化应激水平,改善肝脏组织损伤程度。结论:ATG对糖尿病性肝损伤具有保护作用,本研究可为ATG用于糖尿病性肝损伤的防治提供参考依据。 相似文献
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目的:探究人参皂苷CK对2型糖尿病(T2DM)大鼠肝损伤的保护机制。方法:本试验通过建立T2DM大鼠模型,记录大鼠空腹血糖值(FBG),灌胃8周后进行口服糖耐量(OGTT)测试,检测血清中相关指标,肝组织匀浆中相关指标以及四种炎性因子的水平,苏木精-伊红(HE)染色法检测肝组织病变情况,Western Blot法检测TLR/Myd88/NF-κB信号通路蛋白的表达。结果:人参皂苷CK组能够显著的降低T2DM大鼠的FBG水平(P<0.05),恢复其糖耐量水平,显著提高总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)、谷丙转氨酶(ALT)、谷草转氨酶(AST)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、过氧化氢酶(CAT)水平(P<0.05),显著降低高密度脂蛋白(HDL-C),丙二醛(MDA),四种炎性因子以及Toll样受体4(TLR4)、髓样分化因子(Myd88)、细胞核因子(p65)和大鼠核因子κB抑制蛋白α(p-IκB-α)蛋白的表达水平(P<0.05),恢复肝组织形态结构。结论:人参皂苷CK能够通过降低炎症以及氧化应激反应从而保护T2DM大鼠的肝损伤情况,并调控TLR/Myd88/NF-κB信号通路。 相似文献
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Eun-Kyeong Lee Do-Won Jeong Se Jin Lim Gyo-Jeong Gu Sang-Il Ahn Ji-Soo Kim Ji Hun Paek Songmun Kim Jae Seung Hong Soon Sung Lim Hyung-Sun Youn 《Food science and biotechnology》2014,23(5):1637-1641
Inflammation is a pathological and physiological process which is known to be involved in numerous diseases, while it is notable that a considerable proportion of chronic inflammatory diseases overlap with the development of cancer. One of the most important proteins for inflammatory responses is inducible nitric oxide synthase (iNOS). The present study investigated the effect of the extract of Carpesium abrotanoides L. (ECA) on inflammation by modulating iNOS expression induced by toll-like receptors (TLRs) agonists in murine macrophages. ECA suppressed iNOS expression induced by lipopolysaccharide (TLR4 agonist), macrophage-activating lipopeptide 2-kDa (TLR2 and TLR6 agonist), and polyriboinosinic polyribocytidylic acid (TLR3 agonist). All the results suggest that ECA can modulate TLR signaling pathways and subsequent chronic inflammatory responses. 相似文献
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Susana Figueroa‐Lozano Rivca L. Valk‐Weeber Sander S. van Leeuwen Lubbert Dijkhuizen Paul de Vos 《Molecular nutrition & food research》2018,62(2)
1 Scope
Bovine lactoferrin (bLF) is an ingredient of food supplements and infant formulas given its antimicrobial and antiviral properties. We modified bLF enzymatically to alter its N‐glycosylation and to isolate the glycan chains. The aims of this study include (1) to evaluate whether such derivates induce responses via pattern recognition receptors namely Toll‐like receptors (TLRs) and (2) to relate those responses to their different glycosylation profiles.2 Methods and results
The unmodified and modified bLF fractions are incubated with reporter cell lines expressing pattern recognition receptors. Afterwards, we screen for TLRs and analyze for nuclear factor kappa—light‐chain enhancer of activated B cells (NF‐κB) activation. Activation of reporter cell lines show that signaling is highly dependent on TLRs. The activation pattern of bLF is reduced with the desialylated form and increased with the demannosylated form. In reporter cells for TLR, bLF activate TLR‐4 and inhibit TLR‐3. The isolated glycans from bLF inhibit TLR‐8. TLR‐2, TLR‐5, TLR‐7, and TLR‐9 are not significantly altered.3 Conclusion
The profile of glycosylation is key for the biological activity of bLF. By understanding how this affects the human defense responses, the bLF glycan profile can be modified to enhance its immunomodulatory effects when used as a dietary ingredient. 相似文献11.
目的:研究羊栖菜多酚对脂多糖(lipopolysaccharide,LPS)诱导小鼠单核巨噬细胞白血病细胞RAW264.7细胞炎症反应的影响。方法:噻唑蓝法测定细胞活力;Griess法测定一氧化氮(NO)水平;实时荧光定量聚合酶链式反应测定白细胞介素(interleukin,IL)-6、IL-1β、肿瘤坏死因子(tumor necrosis factor,TNF)-α、环氧合酶2(cyclooxygenase-2,COX-2)和诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)的基因相对表达量;流式细胞术测定细胞吞噬能力;蛋白免疫印迹法测定信号通路丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPKs)和核转录因子(nuclear factor,NF)-κB信号通路关键蛋白表达水平。结果:羊栖菜多酚对RAW264.7细胞的安全质量浓度范围为0~160 μg/mL。与LPS组相比,羊栖菜多酚剂量依赖性降低巨噬细胞吞噬能力并抑制NO的生成。同时,羊栖菜多酚下调促炎细胞因子(IL-1β、IL-6、TNF-α)和炎症诱导酶(iNOS、COX-2)的mRNA水平,且作用效果与给药剂量及LPS刺激时间相关。这些炎性介质的表达与羊栖菜多酚抑制p38 MAPK和NF-κB p65的激活有关。结论:羊栖菜多酚可通过减弱p38 MAPK和NF-κB p65信号通路的激活水平,抑制下游炎症介质的转录表达,从而缓解LPS诱导的巨噬细胞炎症反应。 相似文献
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Shenshen Zhang Shaoping Nie Danfei Huang Wenjuan Li Mingyong Xie 《Food chemistry》2013,136(3-4):1213-1219
Ganoderma atrum has attracted great attention for its antitumor activity. However, the mechanism remains unclear. A G. atrum polysaccharide (PSG-1) showed pronounced antitumor activity in this study. PSG-1 did not kill CT26 cells directly, but inhibited the proliferation of CT26 cells via the activation of peritoneal macrophages (MΦ). In vivo, PSG-1 significantly suppressed the tumor growth in CT26 tumor-bearing mice. The treatment caused a significant increase in the immune organ index and the phagocytosis of macrophages. The production of TNF-α, IL-1β and nitric oxide also increased. Furthermore, we found that PSG-1 acted on Toll-like receptor (TLR) 4, signaled through p38 MAPK pathway, then activated NF-κB and stimulated TNF-α production. We further found that PSG-1 increased the expression of TLR4 and NF-κB, the degradation of IκBα and the phosphorylation of p38 MAPK. In summary, we have demonstrated that PSG-1 could activate macrophages via TLR4-dependent signaling pathways, improve immunity and inhibit tumor growth. 相似文献
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Bovine miR-146a regulates inflammatory cytokines of bovine mammary epithelial cells via targeting the TRAF6 gene 总被引:1,自引:0,他引:1
《Journal of dairy science》2017,100(9):7648-7658
It has been reported previously that bovine miR-146a (bta-miR-146a) is significantly differentially expressed in mammary glands infected with mastitis, compared with healthy udders. This suggests that bta-miR-146a plays an important role in the regulation of mammary inflammation. However, the specifics of this function have yet to be elucidated. Bovine mammary epithelial cells (bMEC) represent the first line of defense against pathogens and have important roles in initiating and regulating inflammatory responses and innate immunity during infection. In this study, a double luciferase reporter assay was used to confirm that bta-miR-146a directly targets the 3′ UTR of the tumor-necrosis factor receptor-associated factor 6 (TRAF6) gene. To elucidate the role of bta-miR-146a in innate immune responses, either a mimic or inhibitor of bta-miR-146a was transfected into bMEC stimulated with lipopolysaccharide, which activates the innate immune response through the toll-like receptor (TLR) 4/nuclear factor (NF)-κB signaling pathway. Forty-eight hours posttransfection, quantitative real-time PCR and Western blots were used to detect the expressions of the related genes and proteins, respectively. An ELISA was used to measure the quantity of inflammatory factors in culture supernatants. The results showed that bta-miR-146a significantly inhibits both mRNA and protein expression levels of bovine TRAF6, and ultimately suppresses downstream expression of NF-κB mRNA and protein. As a result, production of NF-κB-dependent inflammatory mediators such as tumor necrosis factor α, IL-6, and IL-8 are suppressed following lipopolysaccharide stimulation of bMEC. Thus, we concluded that bta-miR-146a acts as a negative feedback regulator of bovine inflammation and innate immunity through downregulation of the TLR4/TRAF6/NF-κB pathway. This study presents a potential regulatory mechanism of bta-miR-146a on immune responses in bovine mammary infection and may provide a potential therapeutic target for mastitis. 相似文献
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食用菌是含有多种生物活性物质的大型真菌,广泛分布于自然界中。许多研究表明,食用菌中的生物活性蛋白具有免疫调节、抗肿瘤、抗菌等功能,尤其是免疫调节活性备受关注。Toll样受体(toll-like receptors,TLRs)信号通路能将细胞外的信号传递到免疫系统中,激活细胞内丝裂原活化蛋白激酶和核因子-κB信号通路。本文综述了食用菌中免疫调节蛋白、凝集素、核糖体失活蛋白、糖肽等生物活性蛋白通过TLRs信号通路调节机体免疫的作用机制,为深入了解食用菌活性蛋白的功能活性,开发食用真菌保健食品或药品提供参考。 相似文献
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细胞焦亡是细胞促炎程序性死亡,其强弱程度依赖于胱天蛋白酶(Caspases)活性。Caspases通过切割Gasdermin家族蛋白使其形成无活性的C端片段和有活性的N端片段,后者移位到膜上并形成穿孔,导致水分渗透和细胞肿胀并释放炎性因子,继而引发细胞焦亡。细胞焦亡的不同信号通路机制在各类疾病的发生发展过程中发挥着重要作用。多糖作为生物大分子对细胞核因子-κB、核苷酸结合寡聚化结构域样受体蛋白3(NOD-like receptor protein 3,NLRP3)及活性氧等信号分子均具有调节作用。但多糖能否通过影响相关信号通路达到抑制或激活细胞焦亡的作用有待进一步研究。本文综述细胞焦亡相关信号通路、细胞焦亡在疾病中的作用及多糖在细胞焦亡信号通路调节中的作用,旨在对多糖在细胞焦亡中的潜在作用进行探讨,为进一步开发功能性多糖提供新的思路。 相似文献
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单核细胞介导的炎症反应在动脉粥样硬化发生和发展过程中起关键作用。花色苷是一种具有多种生物学活性的多酚类黄酮化合物,富含于各种深色的蔬菜、水果及谷类中,其中矢车菊素-3-O-β-葡萄糖苷(cyanidin-3-O-β-glucoside,Cy-3-g)是花色苷中重要的单体,本研究旨在探讨黑米来源的Cy-3-g对脂多糖(lipopolysaccharide,LPS)诱导的人单核白血病细胞(Tohoku hospital pediatrics-1,THP-1)炎症损伤的作用及可能的分子机制。采用乙醇-盐酸溶液浸提、大孔树脂吸附洗脱等步骤得到黑米花色苷粗提物,然后用中压液相层析联合紫外检测提取得到纯化的Cy-3-g(纯度>96.5%)。用不同质量浓度(0、0.10、0.25μg/mL和0.50μg/mL)Cy-3-g与THP-1细胞共孵育4 h,然后加入LPS(质量浓度50 ng/mL)与细胞继续孵育48 h,用酶联免疫吸附试验法测定培养液中白细胞介素-1β(interleukin-1β,IL-1β)、IL-6、IL-8、IL-10和肿瘤坏死因子-α(tumor necrosis fac... 相似文献
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Ginger is a commonly used spice with anti-inflammatory potential. Colitis is the common pathological lesion of inflammatory bowel diseases. In this study, we investigated the therapeutic effects of ginger and its component zingerone in mice with 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis. Ginger and zingerone ameliorated TNBS-induced colonic injury in a dose-dependent manner. Pathway analysis of ginger- and zingerone-regulated gene expression profiles showed that ginger and zingerone significantly regulated cytokine-related pathways. Network analysis showed that nuclear factor-κB (NF-κB) and interleukin-1β (IL-1β) were key molecules involved in the expression of ginger- and zingerone-affected genes. Ex vivo imaging and immunohistochemical staining further verified that ginger and zingerone suppressed TNBS-induced NF-κB activation and IL-1β protein level in the colon. In conclusion, ginger improved TNBS-induced colitis via modulation of NF-κB activity and IL-1β signalling pathway. Moreover, zingerone might be the active component of ginger responsible for the amelioration of colitis induced by TNBS. 相似文献