scholarly journals Lutonarin from Barley Seedlings Inhibits the Lipopolysacchride-Stimulated Inflammatory Response of RAW 264.7 Macrophages by Suppressing Nuclear Factor-κB Signaling

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1571
Author(s):  
Ji Yeong Yang ◽  
So-Yeun Woo ◽  
Mi Ja Lee ◽  
Hyun Young Kim ◽  
Jin Hwan Lee ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Nuclear Factor Κb ◽  
Ultra Performance Liquid Chromatography ◽  
Raw 264.7 ◽  
Nuclear Factor ◽  
Raw 264.7 Macrophages ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
Necrosis Factor

Extracts from barley seedlings (BS) have known antioxidant and anti-inflammatory activities. The flavonoid lutonarin (LN) is a component of BS extract and has several known bioactivities. Here, we evaluated LN anti-inflammatory efficacy against lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Lutonarin was isolated from BS by methanol extraction and characterized by ultra-performance liquid chromatography and quadrupole time-of-flight tandem mass spectrometry (UPLC-Q-TOF-MS/MS). Lutonarin did not reduce the viability or enhance the apoptosis rate of RAW 264.7 macrophages at concentrations up to 150 µM. Concentrations within 20–60 µM dose-dependently suppressed the LPS-induced expression, phosphorylation, and nuclear translocation of the inflammatory transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). Furthermore, LN suppressed the LPS-induced upregulation of proinflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α and of the inflammatory enzyme cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). Lutonarin may be a safe and effective therapeutic agent for alleviation of pathological inflammation.

scholarly journals Anti-Inflammatory Effects of Ribes diacanthum Pall Mediated via Regulation of Nrf2/HO-1 and NF-κB Signaling Pathways in LPS-Stimulated RAW 264.7 Macrophages and a TPA-Induced Dermatitis Animal Model

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 622
Author(s):  
Na Yeon Kim ◽  
Sun Hee Cheong ◽  
Kun Jong Lee ◽  
Dai-Eun Sok ◽  
Mee Ree Kim
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Nuclear Translocation ◽  
Raw 264.7 Cells ◽  
Heme Oxygenase 1 ◽  
Raw 264.7 ◽  
Nuclear Factor ◽  
Raw 264.7 Macrophages ◽  
Tnf Α ◽  
Anti Inflammatory

Ribes diacanthum Pall (RDP) is a Mongolian traditional medicine used to treat renal inflammation. In the present study, we initially investigated the anti-inflammatory effects and mechanisms of action of ethylacetate extract of RDP (EARDP) in RAW 264.7 macrophages stimulated by lipopolysaccharide (LPS) and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced dermatitis in mice. We demonstrated that EARDP protected against LPS-induced cell death by inhibiting intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) production, as well as the synthesis of pro-inflammatory mediators and cytokines, such as nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β. EARDP inhibited the phosphorylation and degradation of inhibitory κB-α (IκB-α) and the activation of nuclear factor (NF)-κB, indicating that the anti-inflammatory effect of EARDP was mediated via the suppression of NF-κB nuclear translocation. In addition, EARDP induced the heme oxygenase-1 (HO-1) expression and nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2), indicating that EARDP induced HO-1 via the Nrf2 pathway in RAW 264.7 cells. Furthermore, EARDP significantly suppressed the protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-stimulated RAW 264.7 macrophages. However, ZnPP, a specific inhibitor of HO-1, reversed the EARDP-mediated inhibition of NO and TNF-α production in LPS-stimulated RAW 264.7 macrophages. EARDP blocked the phosphorylation of mitogen-activated protein kinase (MAPK) and Akt in LPS-stimulated RAW 264.7 cells. In the in vivo animal model, EARDP significantly and dose-dependently reduced TPA-induced secretion of TNF-α and IL-6 in mouse ear. Based on these results, EARDP represents a promising natural compound, protective against oxidative stress and inflammatory diseases.

scholarly journals Anti-Inflammatory Compounds from Atractylodes macrocephala

Molecules ◽  
2019 ◽  
Vol 24 (10) ◽  
pp. 1859 ◽  
Author(s):  
Dawoon Jeong ◽  
Guang-zhi Dong ◽  
Hwa Jin Lee ◽  
Jae-Ha Ryu
Keyword(s):  
Nitric Oxide ◽  
Nuclear Translocation ◽  
Inflammatory Diseases ◽  
Nuclear Factor Κb ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Mrna Levels ◽  
Anti Inflammatory ◽  
Atractylodes Macrocephala ◽  
Oxide Synthase

In relation to anti-inflammatory agents from medicinal plants, we have isolated three compounds from Atractylodes macrocephala; 1, 2-[(2E)-3,7-dimethyl-2,6-octadienyl]-6-methyl-2, 5-cyclohexadiene-1, 4-dione; 2, 1-acetoxy-tetradeca-6E,12E-diene-8, 10-diyne-3-ol; 3, 1,3-diacetoxy-tetradeca-6E, 12E-diene-8, 10-diyne. Compounds 1–3 showed concentration-dependent inhibitory effects on production of nitric oxide (NO) and prostaglandin E2 (PGE2) in lipopolysaccharide (LPS)-activated RAW 264.7 macrophages. Western blotting and RT-PCR analyses demonstrated that compounds 1–3 suppressed the protein and mRNA levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Furthermore, compounds 1–3 inhibited transcriptional activity of nuclear factor-κB (NF-κB) and nuclear translocation of NF-κB in LPS-activated RAW 264.7 cells. The most active compound among them, compound 1, could reduce the mRNA levels of pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) and suppress the phosphorylation of MAPK including p38, JNK, and ERK1/2. Taken together, these results suggest that compounds 1–3 from A. macrocephala can be therapeutic candidates to treat inflammatory diseases.

scholarly journals Anti-Inflammatory Activity and ROS Regulation Effect of Sinapaldehyde in LPS-Stimulated RAW 264.7 Macrophages

Molecules ◽  
2020 ◽  
Vol 25 (18) ◽  
pp. 4089
Author(s):  
Seung-Hwa Baek ◽  
Tamina Park ◽  
Myung-Gyun Kang ◽  
Daeui Park
Keyword(s):  
Nitric Oxide ◽  
Polymerase Chain Reaction Analysis ◽  
Inos Mrna ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Docking Simulations ◽  
Tnf Α ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Oxide Synthase

We evaluated the anti-inflammatory effects of SNAH in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages by performing nitric oxide (NO) assays, cytokine enzyme-linked immunosorbent assays, Western blotting, and real-time reverse transcription-polymerase chain reaction analysis. SNAH inhibited the production of NO (nitric oxide), reactive oxygen species (ROS), tumor necrosis factor (TNF)-α, and interleukin (IL)-6. Additionally, 100 μM SNAH significantly inhibited total NO and ROS inhibitory activity by 93% (p < 0.001) and 34% (p < 0.05), respectively. Protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) stimulated by LPS were also decreased by SNAH. Moreover, SNAH significantly (p < 0.001) downregulated the TNF-α, IL-6, and iNOS mRNA expression upon LPS stimulation. In addition, 3–100 µM SNAH was not cytotoxic. Docking simulations and enzyme inhibitory assays with COX-2 revealed binding scores of −6.4 kcal/mol (IC50 = 47.8 μM) with SNAH compared to −11.1 kcal/mol (IC50 = 0.45 μM) with celecoxib, a known selective COX-2 inhibitor. Our results demonstrate that SNAH exerts anti-inflammatory effects via suppression of ROS and NO by COX-2 inhibition. Thus, SNAH may be useful as a pharmacological agent for treating inflammation-related diseases.

Anti-Inflammatory Effect of Local Anaesthetic Ropivacaine in Lipopolysaccharide-Stimulated RAW264.7 Macrophages

Pharmacology ◽  
2019 ◽  
Vol 103 (5-6) ◽  
pp. 228-235 ◽  
Author(s):  
Li Wu ◽  
Lu Li ◽  
Fang Wang ◽  
Xianwei Wu ◽  
Xin Zhao ◽  
...  
Keyword(s):  
Significant Inhibition ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Raw264.7 Macrophages ◽  
Tnf Α ◽  
Mitogen Activated Protein ◽  
Anti Inflammatory ◽  
Necrosis Factor ◽  
Inflammatory Effect

The present manuscript intended to investigate the anti-inflammatory effect of ropivacaine on lipopolysaccharide-induced inflammation in RAW 264.7 macrophages. Results suggested that ropivacaine causes significant inhibition of generation of nitric oxide (NO), prostaglandin E2, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β, as well as expression of their synthesizing enzymes, inducible NO synthase, and cyclooxygenase-2. Moreover, ropivacaine causes inhibition of mitogen-activated protein kinases as well as nuclear factor-kappa B signaling pathway and apoptosis in RAW 264.7 cells. Based on the results, it has been suggested that ropivacaine showed beneficial effect against inflammation.

Monoammonium glycyrrhizate suppresses tumor necrosis factor-α induced chemokine production in HMEC-1 cells, possibly by blocking the translocation of nuclear factor-κB into the nucleus

2014 ◽  
Vol 92 (10) ◽  
pp. 859-865 ◽  
Author(s):  
Na Cao ◽  
Tao Chen ◽  
Zai-pei Guo ◽  
Sha Qin ◽  
Meng-meng Li
Keyword(s):  
Tumor Necrosis ◽  
Skin Diseases ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Inflammatory Skin Diseases ◽  
Chemokine Production ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Necrosis Factor

Monoammonim glycyrrhizate (MAG) derived from licorice has been shown to have anti-inflammatory properties. Chemokines are vital inflammatory mediators that are involved with endothelial damage from leukocyte infiltrates in various inflammatory skin diseases. In this study, we investigated the anti-inflammatory effects and mechanisms of MAG on tumor necrosis factor-α (TNF-α) induced chemokine production in a human dermal microvascular endothelial cell line (HMEC-1). HMEC-1 cells were treated with TNF-α, with or without MAG. The results showed that MAG suppressed TNF-α-induced chemokine (including CXCL8, CX3CL1, and CXCL16) mRNA expression in HMEC-1 cells, in a dose-dependent manner, and reduced the secretion of these chemokines in culture supernatant. Moreover, endothelial activation in the presence of MAG blocked the chemotactic activities of TNF-α-stimulated HMEC-1 cell supernatant on the migration of primary neutrophils and primary monocytes. In addition, Western blot and immunofluorescence data revealed that MAG inhibited nuclear translocation of nuclear factor-κB p65 (NF-κB p65). It is the first report to demonstrate that MAG suppresses TNF-α-induced chemokine production in HMEC-1 cells, and that the mechanism may be inhibiting the translocation of NF-κB p65 into the nucleus to prevent the starting of inflammatory signaling pathway. Our results revealed that MAG is a potential anti-inflammatory agent capable of improving inflammatory skin diseases.

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