scholarly journals Sargassum Fusiforme Polysaccharide SFP-F2 Activates the NF-κB Signaling Pathway via CD14/IKK and P38 Axes in RAW264.7 Cells

Marine Drugs ◽  
2018 ◽  
Vol 16 (8) ◽  
pp. 264 ◽  
Author(s):  
Liujun Chen ◽  
Peichao Chen ◽  
Jian Liu ◽  
Chenxi Hu ◽  
Shanshan Yang ◽  
...  
Keyword(s):  
Immune Response ◽  
Signaling Pathway ◽  
Biological Activities ◽  
Raw264.7 Cells ◽  
Enhancement Effect ◽  
Sargassum Fusiforme ◽  
Pathway Data ◽  
Tnf Α ◽  
Immune Enhancement ◽  
Specific Inhibitors

Sargassum fusifrome is considered a “longevity vegetable” in Asia. Sargassum fusifrome polysaccharides exhibit numerous biological activities, specially, the modulation of immune response via the NF-κB signaling pathway. However, the precise mechanisms by which these polysaccharides modulate the immune response through the NF-κB signaling pathway have not been elucidated. In this study, we purified and characterized a novel fraction of Sargassum fusifrome polysaccharide and named it SFP-F2. SFP-F2 significantly upregulated the production of the cytokines TNF-α, IL-1β and IL-6 in RAW264.7 cells. It also activated the NF-κB signaling pathway. Data obtained from experiments carried out with specific inhibitors (PDTC, BAY 11-7082, IKK16 and SB203580) suggested that SFP-F2 activated the NF-κB signaling pathway via CD14/IKK and P38 axes. SFP-F2 could therefore potentially exert an immune-enhancement effect through inducing the CD14/IKK/NF-κB and P38/NF-κB signaling pathways.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

scholarly journals MiR-155/GSK-3β mediates anti-inflammatory effect of Chikusetsusaponin IVa by inhibiting NF-κB signaling pathway in LPS-induced RAW264.7 cell

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yi Xin ◽  
Qin Yuan ◽  
Chaoqi Liu ◽  
Changcheng Zhang ◽  
Ding Yuan
Keyword(s):  
Signaling Pathway ◽  
Mouse Liver ◽  
Inflammatory Responses ◽  
Biological Activities ◽  
Raw264.7 Cells ◽  
Inflammation Model ◽  
Raw264.7 Cell ◽  
Anti Inflammatory ◽  
Gsk 3Β ◽  
Inflammatory Effect

Abstract It has been demonstrated that Chikusetsusaponin IVa (CsIVa) possesses abundant biological activities. Herein, using LPS to establish acute inflammation model of mouse liver and cell line inflammation model, we investigated whether miR-155/GSK-3β regulated NF-κB signaling pathway, and CsIVa exerted anti-inflammatory effects by regulating miR-155/GSK-3β signaling pathway. Our results showed that LPS induced high expression of miR-155 and miR-155 promoted macrophage activation through GSK-3β. In addition, CsIVa inhibited inflammatory responses in LPS-induced mouse liver and RAW264.7 cells. Furthermore, we demonstrated that CsIVa improved the inflammatory response in LPS-induced RAW264.7 cells by inhibiting miR-155, increasing GSK-3β expression, and inhibiting NF-κB signaling pathway. In conclusion, our study reveals that CsIVa suppresses LPS-triggered immune response by miR-155/GSK-3β-NF-κB signaling pathway.

scholarly journals Anti-Inflammatory Effects of Berchemia floribunda in LPS-Stimulated RAW264.7 Cells through Regulation of NF-κB and MAPKs Signaling Pathway

Plants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 586
Author(s):  
Hyun Ji Eo ◽  
Jun Hyuk Jang ◽  
Gwang Hun Park
Keyword(s):  
Signaling Pathway ◽  
Inflammatory Activity ◽  
Nuclear Accumulation ◽  
Raw264.7 Cells ◽  
No Production ◽  
Tnf Α ◽  
Inflammatory Drugs ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Berchemia floribunda (Wall.) Brongn. (BF), which belongs to Rhamnaceae, is a special plant of Anmyeon Island in Korea. BF has been reported to have antioxidant and whitening effects. However, the anti-inflammatory activity of BR has not been elucidated. In this study, we evaluated the anti-inflammatory effect of leaves (BR-L), branches (BR-B) and fruit (BR-F) extracted with 70% ethanol of BR and elucidated the potential signaling pathway in LPS-induced RAW264.7 cells. BR-L showed a strong anti-inflammatory activity through the inhibition of NO production. BR-L significantly suppressed the production of the pro-inflammatory mediators such as iNOS, COX-2, IL-1β, IL-6 and TNF-α in LPS-stimulated RAW264.7 cells. BR-L suppressed the degradation and phosphorylation of IκB-α, which contributed to the inhibition of p65 nuclear accumulation and NF-κB activation. BR-L obstructed the phosphorylation of MAPKs (ERK1/2, p38 and JNK) in LPS-stimulated RAW264.7 cells. Consequently, these results suggest that BR-L may have great potential for the development of anti-inflammatory drugs to treat acute and chronic inflammatory disorders.

scholarly journals Immune-Enhancement and Anti-Inflammatory Activities of Fatty Acids Extracted from Halocynthia aurantium Tunic in RAW264.7 Cells

Marine Drugs ◽  
2018 ◽  
Vol 16 (9) ◽  
pp. 309 ◽  
Author(s):  
Chaiwat Monmai ◽  
Seok Go ◽  
II-Shik Shin ◽  
Sang You ◽  
Hyungjae Lee ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Saturated Fatty Acids ◽  
Biologically Active ◽  
Raw264.7 Cells ◽  
Macrophage Cells ◽  
Tnf Α ◽  
Immune Enhancement ◽  
Cox 2 ◽  
Anti Inflammatory

Halocynthia aurantium, an edible ascidian species, has not been studied scientifically, even though tunicates and ascidians are well-known to contain several unique and biologically active materials. The current study investigated the fatty acid profiles of the H. aurantium tunic and its immune-regulatory effects on RAW264.7 macrophage cells. Results of the fatty acid profile analysis showed a difference in ratios, depending on the fatty acids being analysed, including those of saturated fatty acids (SFA), monounsaturated fatty acids (MUFA), and polyunsaturated fatty acids (PUFA). In particular, omega-3 fatty acids, such as eicosatrienoic acid n-3 (ETA n-3), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), were much higher than omega-6 fatty acids. Moreover, the H. aurantium tunic fatty acids, significantly and dose-dependently, increased the NO and prostaglandin E2 (PGE2) production in RAW264.7 cells, for immune-enhancement without cytotoxicity. In addition, these fatty acids regulated the transcription of immune-associated genes, including iNOS, IL-1β, IL-6, COX-2, and TNF-α. These actions were activated and deactivated via Mitogen-activated protein kinase (MAPK)and NF-κB signaling, to regulate the immune responses. Conversely, the H. aurantium tunic fatty acids effectively suppressed the inflammatory cytokine expressions, including iNOS, IL-1β, IL-6, COX-2, and TNF-α, in LPS-stimulated RAW264.7 cells. Productions of COX-2 and PGE2, which are key biomarkers for inflammation, were also significantly reduced. These results elucidated the immune-enhancement and anti-inflammatory mechanisms of the H. aurantium tunic fatty acids in macrophage cells. Moreover, the H. aurantium tunic might be a potential fatty acid source for immune-modulation.

scholarly journals β-Ecdysterone Prevents LPS-Induced Osteoclastogenesis by Regulating NF-κB Pathway in Vitro

2020 ◽  
Author(s):  
Yuling Li ◽  
Jing Zhang ◽  
Caiping Yan ◽  
Qian Chen ◽  
Chao Xiang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Herbal Medicines ◽  
Bone Destruction ◽  
Osteoclast Formation ◽  
Raw264.7 Cells ◽  
Chinese Herbal ◽  
Tnf Α ◽  
Orthopedic Diseases ◽  
Pro Inflammatory Cytokines

Abstract BackgroundLipopolysaccharide (LPS), a bacteria product, plays an important role in orthopedic diseases. Drugs that inhibit LPS-induced osteoclastogenesis are urgently needed for the prevention of bone destruction.MethodsIn this study, we evaluated the effect of β-ecdysterone (β-Ecd), a major component of Chinese herbal medicines derived from the root of Achyranthes bidentata BI on LPS-induced osteoclastogenesis in vitro and explored the mechanism underlying the effects of β-Ecd on this.ResultsWe showed that β-Ecd inhibited LPS-induced osteoclast formation from osteoclast precursor RAW264.7 cells. The inhibition occurred through suppressing the production of osteoclast activating TNF-α, IL-1β, PGE2 and COX-2, which led to down-regulating expression of osteoclast-related genes including RANK, TRAF6, MMP-9, CK and CAⅡ. Besides, β-Ecd treatment can inhibit LPS-induced activation of NF-κB signaling pathway in RAW264.7 cells. Meanwhile, inhibition of NF-κB signaling pathway decreased the formation of osteoclasts and expression of pro-inflammatory cytokines which LPS-induced. Collectively, β-Ecd can prevent LPS-induced osteoclast formation in vitro by regulating NF-κB signaling pathway.ConclusionsThese findings provide evidences that β-Ecd might be beneficial as a valuable choice for the prevention and treatment of bacteria-induced bone destruction disease, and give new insights for understanding its possible mechanism.

scholarly journals Nuezhenide Exerts Anti-Inflammatory Activity through the NF-κB Pathway

2020 ◽  
Vol 14 (1) ◽  
pp. 101-111
Author(s):  
Qin-Qin Wang ◽  
Shan Han ◽  
Xin-Xing Li ◽  
Renyikun Yuan ◽  
Youqiong Zhuo ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Biological Activities ◽  
Immunofluorescence Assay ◽  
Inflammatory Activity ◽  
Raw264.7 Cells ◽  
Phosphorylated Proteins ◽  
Tnf Α ◽  
Antioxidative Effects ◽  
Anti Inflammatory ◽  
Ilex Pubescens

Background: Nuezhenide (NZD), an iridoid glycoside isolated from Ilex pubescens Hook. & Arn. var. kwangsiensis Hand.-Mazz. used as a traditional Chinese medicine of clearing away heat and toxic materials, displays a variety of biological activities like anti-tumor, antioxidant, and protecting live. However, few studies involving anti-inflammatory activity and mechanism of NZD are reported. In the present study, NZD’s anti-inflammatory and antioxidative effects were illustrated. Objective: This study aims to test the hypothesis that NZD suppresses LPS-induced inflammation by targeting the NF-κB pathway in RAW264.7 cells. Methods: LPS-stimulated RAW264.7 cells were employed to detect the effect of NZD on cytokine releases by ELISA. Protein expression levels of related molecular markers were quantitated by western blotting analysis. The levels of ROS, NO, and Ca2+ were detected by the flow cytometry. The changes in mitochondrial reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were observed and verified by a fluorescence microscopy. Using immunofluorescence assay, the translocation of NF-κB/p65 from the cytoplasm into the nucleus was determined by a confocal microscopy. Results: NZD exhibited anti-inflammatory activity and reduced the release of inflammatory cytokines such as nitrite, TNF-α, and IL6. NZD suppressed the expression of the phosphorylated proteins like IKKα/β, IκBα, and p65. In addition, the flow cytometry results indicated that NZD inhibited the levels of ROS, NO, and Ca2+ in LPS-stimulated RAW264.7 cells. JC-1 assay data showed that NZD reversed LPS-induced MMP loss. Furthermore, NZD suppressed LPS-induced NF-B/p65 translocation from the cytoplasm into the nucleus. Conclusions: NZD exhibits anti-inflammatory effects via the NF-κB pathway in RAW264.7 cells.

scholarly journals Pseurotin D Inhibits the Activation of Human Lymphocytes

2021 ◽  
Vol 22 (4) ◽  
pp. 1938
Author(s):  
Daniela Rubanova ◽  
Petra Dadova ◽  
Ondrej Vasicek ◽  
Lukas Kubala
Keyword(s):  
Immune Response ◽  
T Cells ◽  
B Cells ◽  
T Cell Activation ◽  
Cell Activation ◽  
Biological Activities ◽  
Human Lymphocytes ◽  
Future Research ◽  
Activation Markers ◽  
Tnf Α

Background: Pseurotins, a family of secondary metabolites of different fungi characterized by an unusual spirocyclic furanone-lactam core, are suggested to have different biological activities including the modulation of immune response. Purpose: Complex characterization of the effects of pseurotin D on human lymphocyte activation in order to understand the potential of pseurotin to modulate immune response in humans. Methods: CD4+ and CD8+ T cells and CD19+ B cells isolated from human blood were activated by various activators simultaneously with pseurotin D treatment. The effects of pseurotin were tested on the basis of changes in cell viability, apoptosis, activation of signal transducers and activators of transcription (STAT) signaling pathways, production of tumor necrosis factor (TNF)-α by T cells, expression of activation markers CD69 and CD25 on T cells and Human Leukocyte Antigen–DR isotype (HLA-DR) on B cells, and the differentiation markers CD20, CD27, CD38, and immunoglobulin (Ig) D on B cells. Results: Pseurotin D significantly inhibited the activation of both CD4+ and CD8+ human T cells complemented by the inhibition of TNF-α production without significant acute toxic effects. The Pseurotin D-mediated inhibition of T-cell activation was accompanied by the induction of the apoptosis of T cells. This corresponded with the inhibited phosphorylation of STAT3 and STAT5. In human B cells, pseurotin D did not significantly inhibit their activation; however, it affected their differentiation. Conclusions: Our results advance the current mechanistic understanding of the pseurotin-induced inhibition of lymphocytes and suggest pseurotins as new attractive chemotypes for future research in the context of immune-modulatory drugs.

scholarly journals Immunomodulatory Effects of N-Acetyl Chitooligosaccharides on RAW264.7 Macrophages

Marine Drugs ◽  
2020 ◽  
Vol 18 (8) ◽  
pp. 421
Author(s):  
Jun-Jin Deng ◽  
Zong-Qiu Li ◽  
Ze-Quan Mo ◽  
Shun Xu ◽  
He-Hua Mao ◽  
...  
Keyword(s):  
Degree Of Polymerization ◽  
Raw264.7 Cells ◽  
No Production ◽  
Immunomodulatory Effects ◽  
New Production ◽  
Single Degree ◽  
Chitosan Oligosaccharides ◽  
Raw264.7 Macrophages ◽  
Tnf Α ◽  
Immune Enhancement

The ongoing development of new production methods may lead to the commercialization of N-acetyl chitooligosaccharides (NACOS), such as chitosan oligosaccharides (COS). The bioactivity of NACOS, although not well detailed, differs from that of COS, as they have more acetyl groups than COS. We used two enzymatically produced NACOS with different molecular compositions and six NACOS (NACOS1–6) with a single degree of polymerization to verify their immunomodulatory effects on the RAW264.7 macrophage cell line. We aimed to identify any differences between COS and various NACOS with a single degree of polymerization. The results showed that NACOS had similar immune enhancement effects on RAW264.7 cells as COS, including the generation of reactive oxygen species (ROS), phagocytotic activity, and the production of pro-inflammation cytokines (IL-1β, IL-6, and TNF-α). However, unlike COS and lipopolysaccharide (LPS), NACOS1 and NACOS6 significantly inhibited nitric oxide (NO) production. Besides their immune enhancement effects, NACOS also significantly inhibited the LPS-induced RAW264.7 inflammatory response with some differences between various polymerization degrees. We confirmed that the NF-κB pathway is associated with the immunomodulatory effects of NACOS on RAW264.7 cells. This study could inform the application of NACOS with varying different degrees of polymerization in human health.

scholarly journals Farrerol Ameliorates TNBS-Induced Colonic Inflammation by Inhibiting ERK1/2, JNK1/2, and NF-κB Signaling Pathway

2018 ◽  
Vol 19 (7) ◽  
pp. 2037 ◽  
Author(s):  
Xin Ran ◽  
Yuhang Li ◽  
Guangxin Chen ◽  
Shoupeng Fu ◽  
Dewei He ◽  
...  
Keyword(s):  
Protective Effect ◽  
Therapeutic Agent ◽  
Biological Activities ◽  
Raw264.7 Cells ◽  
Trinitrobenzene Sulfonic Acid ◽  
Colonic Inflammation ◽  
Tnf Α ◽  
Cox 2 ◽  
Antibacterial And Antioxidant Activity ◽  
Colitis Model

Farrerol, a type of 2, 3-dihydro-flavonoid, is obtained from Rhododendron. Previous studies have shown that Farrerol performs multiple biological activities, such as anti-inflammatory, antibacterial, and antioxidant activity. In this study, we aim to investigate the effect of Farrerol on colonic inflammation and explore its potential mechanisms. We found that the effect of Farrerol was evaluated via the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model in mice and found that Farrerol has a protective effect on TNBS-induced colitis. Farrerol administration significantly improved the weight change, clinical scores, colon length, and intestinal epithelium barrier damage and markedly decreased the inflammatory cytokines production in TNBS-induced mice. The protective effect of Farrerol was also observed in LPS-induced RAW264.7 cells. We found that Farrerol observably reduced the production of inflammatory mediators including IL-1β, IL-6, TNF-α, COX-2, and iNOS in LPS-induced RAW264.7 cells via suppressing AKT, ERK1/2, JNK1/2, and NF-κB p65 phosphorylation. In conclusion, the study found that Farrerol has a beneficial effect on TNBS-induced colitis and might be a natural therapeutic agent for IBD treatment.

TNF-α in Combination with Palmitate Enhances IL-8 Production via TLR4-Dependent Signaling Pathway—Potential Relevance to Metabolic Inflammation

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1730-P
Author(s):  
RASHEED AHMAD ◽  
NADEEM AKHTER ◽  
SHIHAB P. KOCHUMON ◽  
AREEJ ABU ALROUB ◽  
REEBY S. THOMAS ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Metabolic Inflammation ◽  
Tnf Α ◽  
Dependent Signaling Pathway
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