肾上腺素对小鼠巨噬细胞中促炎／抗炎介质比值的影响

目的：研究肾上腺素对脂多糖（LPS）诱导的小鼠单核巨噬细胞株RAW264.7中促炎介质［肿瘤坏死因子（TNF-α）、一氧化氮（NO）、环加氧酶-2（COX-2）］和抗炎介质［血红素氧化酶-1（HO-1）、白介素10（IL-10）］表达及NF-κB活化的影响。 方法： 以10 μg/L的LPS刺激体外培养的RAW264.7细胞作为炎症模型，加入不同浓度的肾上腺素（1、5、10、50 μmol/L）孵育24 h后，收集培养上清并提取细胞总蛋白，酶联免疫法测定上清中TNF-α、IL-10浓度，Griess法检测上清NO含量(以NO2-/NO3-表示)，免疫印迹法检测细胞总蛋白中COX-2、HO-1、IκB-α的含量。 结果： 10 μg/L的LPS明显诱导TNF-α、NO(NO2-/NO3-)、COX-2、IL-10及HO-1的产生；LPS+肾上腺素组与LPS单独作用组相比促炎介质TNF-α、NO(NO2-/NO3-)、COX-2的表达量显著下降，而抗炎介质IL-10、HO-1的表达却明显增强；肾上腺素与LPS共同作用组中IκB-α的含量与单独LPS作用组相比无明显差异。 结论： 肾上腺素下调LPS诱导的巨噬细胞中促炎介质的表达同时促进抗炎介质的表达，这种效应并不通过影响NF-κB的活化来实现。     

Anti-Inflammatory Mechanism of a Folk Herbal Medicine,Duchesnea indica (Andr) Focke at RAW264.7 Cell Line

This study is to explore the anti-inflammatory mechanism of the ethanol extract of Duchesnea indica (Andr) Focke. An inflammatory cellular model was established by addition of lipopolysaccharide (LPS) on RAW264.7 cell line. The cellular secretion of TNF-α, IL-1β, IL-6, NO and IL-10 in supernatant, mRNA expression of TNF-α, COX-2, iNOS and HO-1, protein expression of COX-2 and HO-1, and activation of NF-κB were assayed by ELISA, the Griess method, real-time quantitative PCR, and Western blot and immunocytochemistry method, respectively. The ethanol extract of D. indica not only reduced production of pro-inflammatory cytokines and mediators and blocked NF-κB activation, but also slightly promoted release of the anti-inflammatory mediator HO-1 and suppressed IL-10 secretion. In conclusion, the anti-inflammatory effects of the extract of D. indica are attributed to the suppression of pro-inflammatory cytokines and mediators by blocking NF-κB activation. The extract of D. indica can also slightly promote HO-1 production to reduce inflammation.     

β-sitosteryl-3-O-β-glucopyranoside isolated from the bark of Sorbus commixta ameliorates pro-inflammatory mediators in RAW 264.7 macrophages

The bark of Sorbus commixta has been used in Asian traditional medicine for treatment of cough, asthma, bronchial disorders, gastritis and dropsy. However, the anti-inflammatory effect of β-sitosteryl-3- O -β-glucopyranoside, a major compound of the bark of S. commixta, is poorly understood. In this study, we investigated the anti-inflammatory effect and the underlying molecular mechanisms of β-sitosteryl-3-O-β-glucopyranoside in lipopolysaccharide (LPS)-induced RAW 264.7 cells. Prostaglandin E₂ (PGE₂) and cytokines released from cells were measured using EIA assay kit. The expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2, Tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) was measured by real-time polymerase chain reaction (RT-PCR) and/or Western blot analysis. β-sitosteryl-3-O-β-glucopyranoside inhibited the production of nitric oxide (NO) and PGE₂ along with the expression of iNOS and COX-2 in LPS-stimulated RAW264.7 cells. In addition, β-sitosteryl-3-O-β-glucopyranoside reduced the release of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6. Moreover, β-sitosteryl-3-O-β-glucopyranoside inhibited the NF-κB activation induced by LPS, which was associated with the abrogation of IκBα degradation and subsequent decreases in nuclear p65 levels. The result suggested that the β-sitosteryl-3-O-β-glucopyranoside inhibited NO and pro-inflammatory productions by down-regulating the gene expression of pro-inflammatory mediators via the negative regulation of the NF-кB pathway in LPS-stimulated RAW 264.7 cells.     

黄连乙醇提取物与盐酸小檗碱体外抗炎对比研究

目的:比较黄连乙醇提取物与盐酸小檗碱体外抗炎活性,探索体外抗炎机制。方法:通过脂多糖体外刺激小鼠单核巨噬细胞建立细胞炎症模型,给药干预后,LPS 长时间刺激RAW264.7 细胞,MTT 比色法分析黄连乙醇提取物及盐酸小檗碱对RAW264.7 细胞生长活性的影响。酶联免疫吸附法检测细胞上清液中IL-β、IL-6、TNF-α、NO、前列腺素E2 (PGE2)含量。实时荧光定量RT-PCR 法检测iNos、HO-1、TNF-αmRNA 表达。结果:在5 ~80 mg/ L 范围内,黄连乙醇提取物及盐酸小檗碱对RAW264.7 细胞无抑制作用;各浓度给药组IL-6、IL-1β、TNF-α、NO、前列腺素E2 (PGE2 )含量与LPS 刺激模型组比较均有显著性(P<0.01),且浓度与剂量无效应相关。实时荧光定量RT-PCR 结果显示,各浓度给药组均明显降低iNos、HO-1、TNF-αmRNA 表达(P<0.05,P<0.05,P<0.01),且与浓度不呈效应关系。结论:黄连乙醇提取物具有体外抗炎作用,抗炎活性优于盐酸小檗碱,其作用机制可能与抑制TNF-α、NO 等炎症因子的活化,进而影响花生四烯酸(AA)代谢有关。     

p-Cymene Modulates In Vitro and In Vivo Cytokine Production by Inhibiting MAPK and NF-κB Activation

The present study was designed to investigate the effects of p-cymene on lipopolysaccharide (LPS)-induced inflammatory cytokine production both in vitro and in vivo. The production of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-10 (IL-10) in LPS-stimulated RAW 264.7 cells and C57BL/6 mice was evaluated by sandwich ELISA. Meanwhile, the mRNA levels of cytokine genes were examined in vitro by semiquantitative RT-PCR. In a further study, we analyzed the activation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways by western blotting. We found that p-cymene significantly regulated TNF-α, IL-1β, and IL-6 production in LPS-stimulated RAW 264.7 cells. Furthermore, the levels of relative mRNAs were also found to be downregulated. In in vivo trail, p-cymene markedly suppressed the production of TNF-α and IL-1β and increased IL-10 secretion. We also found that p-cymene inhibited LPS-induced activation of extracellular signal receptor-activated kinase 1/2, p38, c-Jun N-terminal kinase, and IκBα. These results suggest that p-cymene may have a potential anti-inflammatory action on cytokine production by blocking NF-κB and MAPK signaling pathways.     

Cepharanthine, an Alkaloid from Stephania cepharantha Hayata, Inhibits the Inflammatory Response in the RAW264.7 Cell and Mouse Models

The aim of this study was to investigate the protective effects of cepharanthine (CEP) on inflammation in lipopolysaccharide (LPS)-stimulated RAW264.7 cells in vitro and a LPS-induced lung injury model in vivo. RAW264.7 cells were treated with various concentrations of CEP for 1 h followed by incubation with or without 1 μg/ml LPS for 18 h. TNF-α, IL-6, and IL-1β in the supernatants were measured by ELISA. Nuclear factor-κB (NF-κB) and mitogen-activated protein kinase pathways were analyzed by Western blot. Mice were randomly divided into control group, LPS group, CEP?+?LPS group, and dexamethasone?+?LPS group. A male BALB/c mouse model of acute lung injury was induced by LPS. Bronchoalveolar lavage fluid was collected for inflammatory cell count and cytokine assays. Histopathologic examination was performed on mice that were not subjected to bronchoalveolar lavage fluid collection. CEP dose-dependently inhibited the release of TNF-α, IL-6, and IL-1β in LPS-stimulated RAW264.7 cells. Significantly, CEP dose-dependently suppressed NF-κB activation, IκBα degradation, and phosphorylation of ERK, JNK, and p38 induced by LPS. In vivo, it was also observed that CEP attenuated lung histopathologic changes and down-regulated the level of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, in the mouse acute lung injury model. These results suggest that CEP potentially decreases inflammation in vitro and in vivo and might be a therapeutic agent against inflammatory diseases.     

Pyranocoumarins Isolated from Peucedanum praeruptorum Dunn Suppress Lipopolysaccharide-Induced Inflammatory Response in Murine Macrophages Through Inhibition of NF-κB and STAT3 Activation

Praeruptorin C, D, and E (PC, PD, and PE) are three pyranocoumarins isolated from the dried root of Peucedanum praeruptorum Dunn of Umbelliferae. In the present study, we investigated the anti-inflammatory effect of these compounds in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells. Pyranocoumarins significantly inhibited LPS-induced production of nitric oxide, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). The mRNA and protein expressions of inducible nitric oxide synthase, IL-6, and TNF-α were also suppressed by these compounds. Both PD and PE exhibited greater anti-inflammatory activities than PC. Further study showed that pyranocoumarins suppressed the cytoplasmic loss of inhibitor κB-α protein and inhibited the translocation of NF-κB from cytoplasm to nucleus. In addition, pyranocoumarins suppressed LPS-induced STAT3 tyrosine phosphorylation. Taken together, the results suggest that pyranocoumarins may exert anti-inflammatory effects in LPS-stimulated RAW 264.7 macrophages through the inhibition of NF-κB and STAT3 activation.     

葫芦素E对脂多糖诱导RAW264.7巨噬细胞炎症反应的影响及作用机制

分析葫芦素E(CuE)对脂多糖(LPS)诱导的小鼠RAW264.7巨噬细胞炎症反应的影响,研究其抗炎作用的分子机制。采用改良MTT法检测RAW264.7细胞的增殖;以碘化丙锭染色检测CuE对细胞周期的影响;采用细胞内细胞因子染色法分析肿瘤坏死因子(TNF-α)的表达;免疫荧光染色分析胞内Actin的结构;应用免疫印迹法检测CuE对G-肌动蛋白(G-ac-tin)及核转录因子NF-κB核转位的影响。实验结果显示CuE对RAW264.7细胞的增殖具有剂量依赖性抑制作用,并降低细胞内G-actin的水平;CuE明显阻止LPS诱导的细胞伸展和伪足形成,使细胞周期阻滞于G2/M期。同时,CuE还明显抑制LPS活化的RAW264.7细胞表达促炎因子TNF-α,并显著降低LPS诱导的转录因子NF-κB的核转位作用。这些结果表明,CuE通过破坏RAW264.7巨噬细胞的肌动蛋白细胞骨架,引起细胞周期阻滞,并抑制LPS诱导的NF-κB核转位以及TNF-α的表达,从而发挥抗炎作用。     

Dichloromethane Fraction of Laminaria japonica Ethanolic Extract Inhibits Lipopolysaccharide-Induced Nitric Oxide Synthase and Cyclooxygenase-2 Expression in RAW 264.7 Cells via NF-κB Pathway

Strong anti-inflammatory activity has been found in Laminaria japonica dichloromethane fraction (LDF); however, the molecular mechanisms underlying its anti-inflammatory activity are not reported. Our results indicated that LDF inhibited LPS-induced nitric oxide and prostaglandin E(2) production in a dose-dependent manner and suppressed the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) in RAW 264.7 cells. Also, levels of pro-inflammatory cytokines such as tumor necrosis factor-α, interleukin (IL)-1β and IL-6 were remarkably reduced by LDF in LPS-treated RAW 264.7 cells. LDF greatly inhibited promoter activity of nuclear factor-κB (NF-κB) and translocation of NF-κB subunits by prevention of the degradation of inhibitor κB-α in LPS-treated RAW 264.7 cells (p?相似文献   

7,8-Dihydroxyflavone exhibits anti-inflammatory properties by downregulating the NF-κB and MAPK signaling pathways in lipopolysaccharide-treated RAW264.7 cells

7,8-Dihydroxyflavone (7,8-DHF), a member of the flavonoid family, has received considerable attention as a selective tyrosine kinase receptor B agonist. Several studies have indicated that 7,8-DHF has neurotrophic and antioxidant activities. However, little is known about the cellular and molecular mechanisms underlying the anti-inflammatory activity of 7,8-DHF. Therefore, we investigated whether 7,8-DHF affects the expression of inflammatory mediators in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Our results indicated that 7,8-DHF significantly attenuated secretion of LPS-induced inflammatory mediators nitric oxide (NO), prostaglandin E? (PGE?) and interleukin-1β (IL-1β) in RAW264.7 cells. Additionally, LPS-induced expression of inducible NO synthase (iNOS), cyclooxygenase (COX)-2 and IL-1β was decreased by pre-treatment with 7,8-DHF. Our results also showed that 7,8-DHF reduces LPS-induced nuclear factor-κB (NF-κB) activity via the suppression of the nuclear translocation of NF-κB p65 and the degradation of inhibitor κB (lκB). In addition, 7,8-DHF inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) such as extracellular-signal-related kinase (ERK), p38, and c-Jun N-terminal kinase (JNK). These results suggest that the anti-inflammatory property of 7,8-DHF is related to the downregulation of iNOS, COX-2 and IL-1β, due to NF-κB inhibition as well as to the negative regulation of MAPK activation in RAW264.7 cells. Thus, 7,8-DHF may be a novel therapeutic agent for the prevention of various inflammatory diseases.     

槐定碱抑制LPS诱导巨噬细胞株NF-κB表达

 摘 要：目的 观察槐定碱对LPS诱导的RAW264.7巨噬细胞IKKβ,IκBα,NF-κB P65及TNF-α表达的影响,探讨其抗内毒素机制。方法 培养RAW264.7巨噬细胞,分为对照组、槐定碱对照组、LPS组、槐定碱干预组。槐定碱干预组加入LPS100μg/L孵育1h,弃去LPS后加入槐定碱15.63mg/L,作用5、30、60、120min,分别获取细胞与培养液。RT - PCR与Western Blot分别检测NF-κB等的mRNA与蛋白表达,放免法检测培养液中TNF-α含量。结果 LPS组各时间点IKKβ、pIκBα、NF-κB P65 mRNA和/或蛋白表达及TNF-α含量均显著高于同时间点对照组(P < 0.01);槐定碱干预组以上因子mRNA和/或蛋白表达及TNF-α含量均较同时间点LPS组显著回落(P < 0.01)。结论 槐定碱调控LPS激活的巨噬细胞NF-κB通路IKKβ、IκBα、NF-κB P65等分子的表达,进而抑制下游TNF – α分泌是其抗内毒素作用机制之一。     

Chikusetsusaponin V inhibits inflammatory responses via NF-κB and MAPK signaling pathways in LPS-induced RAW 264.7 macrophages

Excessive activation of macrophages is implicated in various inflammation resulted injuries. Saponins from Panax japonicus (SPJ) have been shown to possess anti-inflammatory activities. However, whether Chikusetsusaponin V (CsV), the most abundant component of SPJ, can exert anti-inflammatory activities is unknown. The present study was aimed to investigate the anti-inflammatory effects of CsV in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells and the underlying mechanisms. Our data showed that CsV dose-dependently inhibited NO, iNOS, TNF-α and IL-1β expressions in LPS-stimulated RAW264.7 cells. Increased protein levels of nuclear NF-κB and elevated phosphorylation levels of ERK and JNK in LPS-stimulated RAW 264.7 cells were also found downregulated by CsV treatment. Furthermore, the increase of CD14 and TLR4 mRNA expression due to LPS stimulation were significantly reversed by CsV treatment. These results suggested that CsV attenuated LPS-induced inflammatory responses partly via TLR4/CD14-mediated NF-κB and MAPK pathways.     

Stevioside Suppressed Inflammatory Cytokine Secretion by Downregulation of NF-κB and MAPK Signaling Pathways in LPS-Stimulated RAW264.7 Cells

Stevioside, a diterpene glycoside isolated from Stevia rebaudiana, has been reported to have anti-inflammatory properties. However, the underlying molecular mechanisms are not well understood. The objective of this study was to investigate the molecular mechanism of stevioside in modifying lipopolysaccharide (LPS)-induced signal pathways in RAW264.7 cells. RAW264.7 cells were stimulated with LPS in the presence or absence of stevioside. The expression of pro-inflammatory cytokines was determined by enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction. Nuclear factor-κB (NF-κB), inhibitory kappa B (IκBα) protein, p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) were determined by western blot. The results showed that stevioside dose-dependently inhibited the expression of tumor necrosis factor-α, interleukin-6, and interleukin-1β in LPS-stimulated RAW264.7 cells. Western blot analysis showed that stevioside suppressed LPS-induced NF-κB activation, IκBa degradation, phosphorylation of ERK, JNK, and P38. Our results suggest that stevioside exerts an anti-inflammatory property by inhibiting the activation of NF-κB and mitogen-activated protein kinase signaling and the release of proinflammatory cytokines. These findings suggest that stevioside may be a therapeutic agent against inflammatory diseases.     

Isorhamnetin ameliorates LPS-induced inflammatory response through downregulation of NF-κB signaling

Isorhamnetin, a flavonoid mainly found in Hippophae fhamnoides L. fruit, has been known for its antioxidant activity and its ability to regulate immune response. In this study, we investigated whether isorhamnetin exerts potent antiinflammatory effects in RAW264.7 cell and mouse model stimulated by LPS. The cytokine (TNF-α, IL-1β, and IL-6) levels were determined. In the mouse model of acute lung injury, the phosphorylation of NF-κB proteins was analyzed and inhibitor of NF-κB signaling (PDTC) was used on mice. Our results showed that isorhamnetin markedly decreased TNF-α, IL-1β, and IL-6 concentrations and suppressed the activation of NF-κB signaling. Meanwhile, isorhamnetin reduced the amount of inflammatory cells, the lung wet-to-dry weight ratio, protein leakage, and myeloperoxidase activity. Interference with specific inhibitor revealed that isorhamnetin-mediated suppression of cytokines and protein was via NF-κB signaling. So, it suggests that isorhamnetin might be a potential therapeutic agent for preventing inflammatory diseases.     

Hesperetin Suppresses Inflammatory Responses in Lipopolysaccharide-Induced RAW 264.7 Cells via the Inhibition of NF-κB and Activation of Nrf2/HO-1 Pathways

Hesperetin (Hesp), a common flavanone glycoside, was extracted from the fruit peel of Citrus aurantium L. (Rutaceae). Hesp has been shown to possess various biological properties, including antioxidant, neuroprotective, and anti-inflammatory properties. In this study, we investigated the protective effect of Hesp on inflammatory responses in lipopolysaccharide (LPS)-induced RAW 264.7 cells. Our results indicated that Hesp treatment dramatically suppressed secretion of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β; reduced inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) gene expression; inhibited NF-κB (p65) phosphorylation; and blocked IκBα phosphorylation and degradation. Further studies revealed Hesp markedly enhanced the heme oxygenase (HO)-1 and nuclear factor erythroid 2-related factor 2 (Nrf2) expression, which were involved with inducing Nrf2 nuclear translocation and decreasing Keap1 protein expression. Together, these results indicated that the anti-inflammatory effect of Hesp may be associated with NF-κB inhibition and Nrf2/HO-1 activation.     

Chamomile: an anti-inflammatory agent inhibits inducible nitric oxide synthase expression by blocking RelA/p65 activity

Chamomile has long been used in traditional medicine for the treatment of inflammation-related disorders. In this study we investigated the inhibitory effects of chamomile on nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression, and explored its potential anti-inflammatory mechanisms using RAW 264.7 macrophages. Chamomile treatment inhibited LPS-induced NO production and significantly blocked IL-1β, IL-6 and TNFα-induced NO levels in RAW 264.7 macrophages. Chamomile caused reduction in LPS-induced iNOS mRNA and protein expression. In RAW 264.7 macrophages, LPS-induced DNA binding activity of RelA/p65 was significantly inhibited by chamomile, an effect that was mediated through the inhibition of IKKβ, the upstream kinase regulating NF-κB/Rel activity, and degradation of inhibitory factor-κB. These results demonstrate that chamomile inhibits NO production and iNOS gene expression by inhibiting RelA/p65 activation and supports the utilization of chamomile as an effective anti-inflammatory agent.     

血管紧张素Ⅱ1型受体在脂多糖诱导RAW264.7巨噬细胞促炎性细胞因子产生中的作用

目的 探讨血管紧张素Ⅱ1型受体在脂多糖（LPS）诱导巨噬细胞促炎性细胞因子产生中的作用和机制.方法 按照随机数字表法将小鼠单核巨噬细胞株（RAW264.7）细胞分为空白对照组、ZD7155组、LPS组和LPS ＋ZD7155组.酶联免疫吸附试验法（ELISA）测定各组细胞培养上清液中肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）的含量,逆转录聚合酶链式反应（RT-PCR）检测RAW264.7细胞内TNF-α和IL-1β mRNA表达,凝胶电泳迁移检测法（EMSA）检测RAW264.7细胞内核因子-κB（NF-κB）和活化蛋白-1（AP-1）活性的变化.结果 和空白对照组相比,ZD7155组培养上清液中的TNF-α和IL-1β含量差异没有统计学意义（P＞0.05）,但是LPS组细胞培养上清液中的TNF-α和IL-1β含量均显著高于空白对照组（均P〈0.01）和ZD7155组（均P〈0.05）.LPS组细胞内的TNF-α和IL-1β mRNA表达是空白对照组的2.19倍（P〈0.01）和1.77倍（P〈0.01）,细胞内NF-κB和AP-1活性是空白对照组的1.43倍（P〈0.01）和1.90倍（P〈0.01）.而LPS＋ZD7155组上清液中的TNF-α和IL-1β含量较LPS组下降（均P〈0.05）,细胞内TNF-α和IL-1β mRNA表达较LPS组下降了34.7%（P〈0.01）和49.72%（P〈0.01）,同时细胞内NF-κB活性和AP-1活性较LPS组下降了46.15%（P〈0.05）和48.42%（P〈0.05）.结论 血管紧张素Ⅱ1型受体通过活化转录因子NF-κB和AP-1,参与了LPS诱导巨噬细胞促炎性细胞因子TNF-α和IL-1β的产生和释放.     

Soybean glyceollins mitigate inducible nitric oxide synthase and cyclooxygenase-2 expression levels via suppression of the NF-κB signaling pathway in RAW 264.7 cells

Glyceollins, produced to induce disease resistance responses against specific species, such as an incompatible pathogen Phytophthora sojae in soybeans, have the potential to exhibit anti-inflammatory activity in RAW 264.7 cells. To investigate the anti-inflammatory effects of elicited glyceollins via a signaling pathway, we studied the glyceollin signaling pathway using several assays including RNA and protein expression levels. We found that soybean glyceollins significantly reduced LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production, as well as the expression of inducible ΝΟ synthase (iNOS) and cyclooxygenase-2 (COX-2) via the suppression of NF-κB activation. Glyceollins also inhibited the phosphorylation of IκBα kinase (IKK), the degradation of IκBα, and the formation of NF-κB-DNA binding complex in a dose-dependent manner. Furthermore, they inhibited pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-18, but increased the generation of the anti-inflammatory cytokine IL-10. Collectively, the present data show that glyceollins elicit potential anti-inflammatory effects by suppressing the NF-κB signaling pathway in RAW 264.7 cells.