α-Tocopherol long-chain metabolite α-13’-COOH affects the inflammatory response of lipopolysaccharide-activated murine RAW264.7 macrophages

2015 ◽  
Vol 59 (8) ◽  
pp. 1524-1534 ◽  
Author(s):  
Maria Wallert ◽  
Lisa Schmölz ◽  
Andreas Koeberle ◽  
Verena Krauth ◽  
Michael Glei ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Raw264.7 Macrophages ◽  
Long Chain

scholarly journals Upregulation of miR-150-5p alleviates LPS-induced inflammatory response and apoptosis of RAW264.7 macrophages by targeting Notch1

2020 ◽  
Vol 15 (1) ◽  
pp. 544-552
Author(s):  
Xiaoyan Deng ◽  
Zhixing Lin ◽  
Chao Zuo ◽  
Yanjie Fu
Keyword(s):  
Inflammatory Response ◽  
Underlying Mechanism ◽  
Notch Receptor ◽  
Raw264.7 Cells ◽  
Luciferase Reporter ◽  
Raw264.7 Macrophages ◽  
Factor Α ◽  
Anti Inflammation ◽  
Necrosis Factor ◽  
Dual Luciferase Reporter Assay

AbstractCirculating miR-150-5p has been identified as a prognostic marker in patients with critical illness and sepsis. Herein, we aimed to further explore the role and underlying mechanism of miR-150-5p in sepsis. Quantitative real-time-PCR assay was performed to detect the expression of miR-150-5p upon stimulation with lipopolysaccharide (LPS) in RAW264.7 cells. The levels of tumor necrosis factor-α, interleukin (IL)-6 and IL-1β were measured by ELISA assay. Cell apoptosis was determined using flow cytometry. Western blot was used to assess notch receptor 1 (Notch1) expression in LPS-induced RAW264.7 cells. Dual-luciferase reporter assay was employed to validate the target of miR-150-5p. Our data showed that miR-150-5p was downregulated and Notch1 was upregulated in LPS-stimulated RAW264.7 cells. miR-150-5p overexpression or Notch1 silencing alleviated LPS-induced inflammatory response and apoptosis in RAW264.7 cells. Moreover, Notch1 was a direct target of miR-150-5p. Notch1 abated miR-150-5p-mediated anti-inflammation and anti-apoptosis in LPS-induced RAW264.7 cells. miR-150-5p alleviated LPS-induced inflammatory response and apoptosis at least partly by targeting Notch1 in RAW264.7 cells, highlighting miR-150-5p as a target in the development of anti-inflammation and anti-apoptosis drugs for sepsis treatment.

Rice protein hydrolysates (RPHs) inhibit the LPS-stimulated inflammatory response and phagocytosis in RAW264.7 macrophages by regulating the NF-κB signaling pathway

RSC Advances ◽  
2016 ◽  
Vol 6 (75) ◽  
pp. 71295-71304 ◽  
Author(s):  
Li Wen ◽  
Yuehua Chen ◽  
Li Zhang ◽  
Huixin Yu ◽  
Zhou Xu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Protein Hydrolysates ◽  
Rice Protein ◽  
Phagocytic Ability ◽  
Raw264.7 Macrophages ◽  
Tnf Α

Different RPH components inhibit LPS-induced NO and TNF-α production. RPHs-C-7-3 inhibits the expression of pro-inflammatory expression. RPHs-C-7-3 suppresses the LPS-stimulated phagocytic ability. RPHs-C-7-3 regulates the nuclear translocation of p65.

Flavonoids from sea buckthorn inhibit the lipopolysaccharide-induced inflammatory response in RAW264.7 macrophages through the MAPK and NF-κB pathways

2017 ◽  
Vol 8 (3) ◽  
pp. 1313-1322 ◽  
Author(s):  
Fan Jiang ◽  
Haining Guan ◽  
Danyi Liu ◽  
Xi Wu ◽  
Mingcheng Fan ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Sea Buckthorn ◽  
Raw264.7 Macrophages ◽  
Anti Inflammatory

Seabuckthorn flavonoids (SFs) exerted their anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages by blocking the activation of MAPK and NF-κB.

scholarly journals Momordica charantia Suppresses Inflammation and Glycolysis in Lipopolysaccharide-Activated RAW264.7 Macrophages

Molecules ◽  
2020 ◽  
Vol 25 (17) ◽  
pp. 3783
Author(s):  
Shi Yan Lee ◽  
Won Fen Wong ◽  
Jiyang Dong ◽  
Kian-Kai Cheng
Keyword(s):  
Glucose Metabolism ◽  
Inflammatory Response ◽  
Macrophage Activation ◽  
Nuclear Translocation ◽  
Lactate Production ◽  
Bioactive Compound ◽  
Momordica Charantia ◽  
Activated Macrophages ◽  
Raw264.7 Macrophages ◽  
Tnf Α

Macrophage activation is a key event that triggers inflammatory response. The activation is accompanied by metabolic shift such as upregulated glucose metabolism. There are accumulating evidences showing the anti-inflammatory activity of Momordica charantia. However, the effects of M. charantia on inflammatory response and glucose metabolism in activated macrophages have not been fully established. The present study aimed to examine the effect of M. charantia in modulating lipopolysaccharide (LPS)-induced inflammation and perturbed glucose metabolism in RAW264.7 murine macrophages. The results showed that LPS-induced NF-κB (p65) nuclear translocation was inhibited by M. charantia treatment. In addition, M. charantia was found to reduce the expression of inflammatory genes including IL6, TNF-α, IL1β, COX2, iNOS, and IL10 in LPS-treated macrophages. Furthermore, the data showed that M. charantia reduced the expression of GLUT1 and HK2 genes and lactate production (−28%), resulting in suppression of glycolysis. Notably, its effect on GLUT1 gene expression was found to be independent of LPS-induced inflammation. A further experiment also indicated that the bioactivities of M. charantia may be attributed to its key bioactive compound, charantin. Taken together, the study provided supporting evidences showing the potential of M. charantia for the treatment of inflammatory disorders.

Myrrh mediates haem oxygenase-1 expression to suppress the lipopolysaccharide-induced inflammatory response in RAW264.7 macrophages

2011 ◽  
Vol 63 (9) ◽  
pp. 1211-1218 ◽  
Author(s):  
Yu-Wen Cheng ◽  
Khoot-Peng Cheah ◽  
Che-Wei Lin ◽  
Joe-Sharg Li ◽  
Wen-Yu Yu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Raw264.7 Macrophages ◽  
Haem Oxygenase

Methamphetamine causes neurotoxicity by promoting polarization of macrophages and inflammatory response

2017 ◽  
Vol 37 (5) ◽  
pp. 486-495 ◽  
Author(s):  
X Li ◽  
F Wu ◽  
L Xue ◽  
B Wang ◽  
J Li ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Protein Expression ◽  
Macrophage Polarization ◽  
Enzyme Linked Immunosorbent Assay ◽  
Neuronal System ◽  
Activated Macrophages ◽  
Alternatively Activated Macrophages ◽  
Raw264.7 Macrophages ◽  
Gene And Protein Expression ◽  
Anti Inflammatory

Macrophages, especially their activation state, are closely related to the progression of neurotoxicity. Classically activated macrophages (M1) are proinflammatory effectors, while alternatively activated macrophages (M2) exhibit anti-inflammatory properties. As a powerful addictive psychostimulant drug, coupled with its neurotoxicity, methamphetamine (Meth) abuse may lead to long-lasting abnormalities in the neuronal system. The present study investigated the effect of Meth at subtoxic concentration on macrophage activation state and its underlying toxicity to neuronal cells. PC12 and Murine RAW264.7 cells were coincubated with Meth to test its toxicity. 3-(4,5-Dimethylthiazol)-2,5-diphenyltetrazolium-bromide, enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blot assays were performed to evaluate the toxicity, cytokine secretion, gene, and protein expression. Results showed that cytotoxicity was enhanced on PC12 cells after coculturing with RAW264.7 stimulated with Meth. RAW264.7 macrophages tended to switch to the M1 phenotype, releasing more nitric oxide and proinflammatory cytokines, including tumor necrosis factor α (TNFα), interleukin (IL)-12, and IL-1β, while decreasing the release of anti-inflammatory cytokine IL-10 after treatment with Meth. Meth upregulated the gene expression of IL-6, IL-1β, and TNFα and downregulated the expression of Arg-1, IL-10, and KLF4. Meth could also upregulate the protein expression of IL-1β and TNF α and downregulate the expression of Arg-1 and KLF4. However, the abovementioned effects induced by Meth were abolished by the addition of dopamine receptor D3 antagonist. In conclusion, our study demonstrated that Meth promoted macrophage polarization from M0 to M1 and enhanced inflammatory response, which provided the scientific rationale for the neurotoxicity caused by the chronic use of Meth.

Long-chain fatty alcohols from evening primrose oil inhibit the inflammatory response in murine peritoneal macrophages

2014 ◽  
Vol 151 (1) ◽  
pp. 131-136 ◽  
Author(s):  
S. Montserrat-de la Paz ◽  
M.D. García-Giménez ◽  
M. Ángel-Martín ◽  
M.C. Pérez-Camino ◽  
A. Fernández Arche
Keyword(s):  
Inflammatory Response ◽  
Peritoneal Macrophages ◽  
Fatty Alcohols ◽  
Evening Primrose Oil ◽  
Evening Primrose ◽  
Murine Peritoneal Macrophages ◽  
Long Chain
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