Abstract 353: High Density Lipoprotein Regulates Tumor Necrosis Factor Alpha and Jun Kinase Signaling Pathway in Adipocytes

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Qiaoqing Zhong
Keyword(s):  
Tumor Necrosis ◽  
Density Lipoprotein ◽  
High Density ◽  
Inflammatory Factors ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Necrosis Factor ◽  
Inflammatory Effect

Background: High-density lipoproteins (HDL) is presumed to exhibit cardiovascular protection, since HDL mediate the reverse transport of cholesterol and exhibit strong anti-inflammatory potential. Previous studies have found that HDL can reduce the level of IL-8 secreted by the inflammatory adipocytes, as well as affect the expression of adiponectin and tumor necrosis factor-alpha (TNF-α) under the inflammatory condition in adipocytes. These studies indicate that HDL is closely related to the inflammatory response of adipose tissue, yet its mechanism has not been fully understood. Secretory leucocyte protease inhibitor (SLPI), a nonglycosylated single-chain polypeptide protein, may play an important role in diet-induced obesity and adipocyte inflammation. Purpose: To study the role of SLPI in HDL anti-inflammatory action in the adipocytes, and explore the mechanism of the action. Methods: 3T3-L1 Adipocytes were induced to differentiation and maturation by culturing. Acute inflammation in adipocytes was induced by LPS (100 ng/ml, 6h), and then the adipocytes were pretreated with HDL and/or SLPI-siRNA. The protein and mRNA levels of SLPI, TNF-α and JNK were examined by Western blotting and qRT-PCR assay, respectively. In addition, the levels of inflammatory factors were measured by ELISA. Results: HDL up-regulated SLPI expression, down-regulated TNF-α expression, and inhibited the secretion of inflammatory factors such as IL-1, IL-6, IL-8 and MCP-1 in 3T3-L1 Adipocytes pre-treated by LPS. Silencing of SLPI by its siRNA effectively abolished the anti-inflammatory effect of HDL. JNK inhibitor (SP600125) partially restored the anti-inflammatory effects of HDL decreased by SLPI knockdown and decreased the secretion of inflammatory factors. Conclusions: These data suggest that HDL up-regulate the expression of SLPI and inhibit the inflammation in 3T3-L1 Adipocytes pre-treated by LPS. The anti-inflammatory effect of HDL, including inhibition of the secretion of inflammatory factors via TNF-α/JNK signaling pathway, probably viat up-regulating the SLPI expression. Key words: high-density lipoprotein, Inflammation, Adipocytes

scholarly journals Apigenin-7-Glucuronide from Urera aurantiaca Inhibits Tumor Necrosis Factor Alpha and Total Nitrite Release in Lipopolysaccharide-Activated Macrophages

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Carla Marrassini ◽  
Laura Cogoi ◽  
Valeria Sülsen ◽  
Claudia Anesini
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Maximum Effect ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Necrosis Factor ◽  
Inflammatory Effect

Urera aurantiaca is an Argentinean medicinal and edible species traditionally used to treat symptoms of inflammation. The aim of this study was to evaluate the anti-inflammatory activity of a methanol extract and its major compound. U. aurantiaca aerial parts were extracted with methanol by maceration. A phytochemical analysis was performed, and the extract’s major component, apigenin-7-glucuronide (A7G), was identified by spectroscopic and HPLC methods. The analysis of the inflammatory mediators nitric oxide (NO) and tumor necrosis factor alpha (TNF-α) in lipopolysaccharide- (LPS-) stimulated macrophages were used in the evaluation of the extract and the major compound anti-inflammatory effects. The extract reduced LPS-augmented NO release from 100 μg/mL (27%), reaching the highest inhibition at 1000 μg/mL (96.3%), while A7G reduced it 30.7% at 1 μg/mL, and its maximum effect was 97.1% at 10 μg/mL. In the TNF-α model, the extract at 500 and 1000 μg/mL reduced LPS-augmented TNF-α by 13.5% and 93.9%, respectively; meanwhile, A7G reduced it by 26.2% and 83.8% at 5 and 10 μg/mL, respectively. U. aurantiaca popular use was validated. In the present study, for the first time, A7G was isolated from U. aurantiaca; furthermore, A7G showed anti-inflammatory effect in the macrophage cell line RAW264.7 (ATCC) and seems to be responsible for the extract anti-inflammatory effect.

scholarly journals Suppression of tumor necrosis factor-alpha-induced neutrophil adherence responses by essential oils

2003 ◽  
Vol 12 (6) ◽  
pp. 323-328 ◽  
Author(s):  
Shigeru Abe ◽  
Naho Maruyama ◽  
Kazumi Hayama ◽  
Hiroko Ishibashi ◽  
Shigeharu Inoue ◽  
...  
Keyword(s):  
Essential Oils ◽  
Tumor Necrosis ◽  
Neutrophil Activation ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Neutrophil Adherence ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Necrosis Factor

Background:In aromatherapy, essential oils are used as anti-inflammatory remedies, but experimental studies on their action mechanisms are very limited.Aims:To assess their anti-inflammatory activities, effects of essential oils on neutrophil activation were examinedin vitro.Methods:Neutrophil activation was measured by tumor necrosis factor-alpha (TNF-α)-induced adherence reaction of human peripheral neutrophils.Results:All essential oils tested at 0.1% concentration suppressed TNF-α-induced neutrophil adherence, and, in particular, lemongrass, geranium and spearmint oils clearly lowered the reaction even at 0.0125%. Similar inhibitory activities for the neutrophil adherence were obtained by their major constituent terpenoids: citral, geraniol, citronellol and carvone. In contrast, very popular essential oils, tea tree oil and lavender oil, did not display the inhibitory activity at the concentration.Conclusion:Thus, some essential oils used as anti-inflammatory remedies suppress neutrophil activation by TNF-α at a low concentration (0.0125-0.025%)in vitro.

scholarly journals Azithromycin Selectively Reduces Tumor Necrosis Factor Alpha Levels in Cystic Fibrosis Airway Epithelial Cells

2007 ◽  
Vol 51 (3) ◽  
pp. 975-981 ◽  
Author(s):  
Cristina Cigana ◽  
Baroukh Maurice Assael ◽  
Paola Melotti
Keyword(s):  
Cystic Fibrosis ◽  
Dna Binding ◽  
Tumor Necrosis ◽  
Airway Epithelial ◽  
Necrosis Factor Alpha ◽  
Protein Levels ◽  
Tnf Α ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Necrosis Factor

ABSTRACT Azithromycin (AZM) ameliorates lung function in cystic fibrosis (CF) patients. This macrolide has been suggested to have anti-inflammatory properties as well as other effects potentially relevant for therapy of CF. In this study, we utilized three CF (IB3-1, 16HBE14o- AS3, and 2CFSMEo-) and two isogenic non-CF (C38 and 16HBE14o- S1) airway epithelial cell lines to investigate whether AZM could reduce tumor necrosis factor alpha (TNF-α) mRNA and protein levels by real-time quantitative PCR analysis and an enzyme-linked immunosorbent assay (ELISA), respectively. We studied the effects on the DNA binding of NF-κB and specificity protein 1 (Sp1) by an ELISA. Non-CF cells express significantly lower TNF-α mRNA and protein levels than an isogenic CF cell line. In CF cells, AZM treatment causes a 30% reduction of TNF-α mRNA levels (P < 0.05) and a 45% decrease in TNF-α secretion (P < 0.05), reaching approximately the levels of the untreated isogenic non-CF cells. In CF cells, NF-κB and Sp1 DNA binding activities were also significantly decreased (about 45 and 60%, respectively; P < 0.05) after AZM treatment. Josamycin, a macrolide lacking clinically described anti-inflammatory effects, was ineffective. Finally, AZM did not alter the mRNA expression levels of interleukin-6, a proinflammatory molecule not differentially expressed in CF and isogenic non-CF cells. The results of our study support the anti-inflammatory activities of this macrolide, since we show that AZM reduced the levels of TNF-α and propose inhibitions of NF-κB and Sp1 DNA binding as possible mechanisms of this effect.

scholarly journals Live Lactobacillus reuteri Is Essential for the Inhibitory Effect on Tumor Necrosis Factor Alpha-Induced Interleukin-8 Expression

2004 ◽  
Vol 72 (9) ◽  
pp. 5308-5314 ◽  
Author(s):  
Donglai Ma ◽  
Paul Forsythe ◽  
John Bienenstock
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Lactobacillus Reuteri ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Necrosis Factor

ABSTRACT The mechanism of the apparent anti-inflammatory action of probiotic organisms is unclear. Lactobacillus reuteri is effective in inhibiting colitis in interleukin-10 (IL-10)-deficient mice. Nerve growth factor (NGF), in addition to its activity on neuronal cell growth, has significant anti-inflammatory effects in several experimental systems in vitro and in vivo, including a model of colitis. Our experiments were designed to explore the mechanism of effect of L. reuteri in the human epithelial cell lines T84 and HT29 on cytokine and NGF synthesis and IL-8 response to tumor necrosis factor alpha (TNF-α). Epithelial cells were cultured for various times with live and killed L. reuteri and examined by reverse transcription-PCR for NGF, IL-10, and TNF-α-induced IL-8 expression. An enzyme-linked immunosorbent assay was used to quantitate intracellular IL-8 and secreted product. Western blotting and confocal microscopy were used to determine the effects on IκB and NF-κB, respectively. Live but not heat-killed or gamma-irradiated L. reuteri upregulated NGF and dose dependently inhibited constitutive synthesis by T84 and HT29 cells of IL-8 and that induced by TNF-α in terms of mRNA and intracellular and secreted protein. Similarly, L. reuteri inhibited IL-8 synthesis induced by Salmonella enterica serovar Typhimurium. L. reuteri required preincubation and adherence for effect, inhibited translocation of NF-κB to the nuclei of HeLa cells, and prevented degradation of IκB. Neither cellular lysates nor media supernatants had any effect on TNF-α-induced IL-8. The conclusion is that L. reuteri has potent direct anti-inflammatory activity on human epithelial cells, which is likely to be related to the activity of ingested probiotics. L. reuteri also upregulates an unusual anti-inflammatory molecule, NGF, and inhibits NF-κB translocation to the nucleus.

scholarly journals Association of tumor necrosis factor-alpha -308 G/A and -238 G/A polymorphism with diabetic retinopathy: a systematic review and updated meta-analysis.

2020 ◽  
Author(s):  
Wenna Gao ◽  
Ruilin Zhu ◽  
liu yang
Keyword(s):  
Diabetic Retinopathy ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Meta Analysis ◽  
Entire Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background: Mounting evidence has suggested tumor necrosis factor-alpha (TNF-α) can promote the development of diabetic retinopathy (DR), and TNF-α gene variants may influence DR risk. However, the results are quite different. Objectives: To comprehensively address this issue, we performed the meta-analysis to evaluate the association of TNF-α-308 G/A and -238 G/A polymorphism with DR. Method: Data were retrieved in a systematic manner and analyzed using STATA Statistical Software. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. Allelic and genotypic comparisons between cases and controls were evaluated. Results: For the TNF-α-308 G/A polymorphism, overall analysis suggested a marginal association with DR [the OR(95%CI) of (GA versus GG), (GA + AA) versus GG, and (A versus G) are 1.21(1.04, 1.41), 1.20(1.03, 1.39), and 1.14(1.01, 1.30), respectively]. And the subgroup analysis indicated an enhanced association among the European population. For the TNF-α-238 G/A polymorphism, there was mild correlation in the entire group [the OR(95%CI) of (GA versus GG) is 1.55(1.14,2.11) ], which was strengthened among the Asian population. Conclusion: The meta-analysis suggested that -308 A and -238 A allele in TNF-α gene potentially increased DR risk and showed a discrepancy in different ethnicities.

scholarly journals Anti-Neuroinflammatory and Anti-Inflammatory Activities of Phenylheptatriyne Isolated from the Flowers of Coreopsis lanceolata L. via NF-κB Inhibition and HO-1 Expression in BV2 and RAW264.7 Cells

2021 ◽  
Vol 22 (14) ◽  
pp. 7482
Author(s):  
Hwan Lee ◽  
Zhiming Liu ◽  
Chi-Su Yoon ◽  
Linsha Dong ◽  
Wonmin Ko ◽  
...  
Keyword(s):  
Silica Gel ◽  
Column Chromatography ◽  
Raw264.7 Cells ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Etoac Fraction ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
And Oxidative Stress ◽  
Necrosis Factor

Aging is associated with immune disregulation and oxidative stress which lead to inflammation and neurodegenerative diseases. We have tried to identify the anti-neuroinflammatory and anti-inflammatory components of Coreopsis lanceolata L. The dried flowers of C. lanceolata were extracted with 70% EtOH, and the obtained extract was divided into CH2Cl2, EtOAc, n-BuOH, and H2O fractions. The CH2Cl2 fraction was separated using silica gel and C-18 column chromatography to yield phenylheptatriyne (1), 2′-hydroxy-3,4,4′-trimethoxychalcone (2), and 4′,7-dimethoxyflavanone (3). Additionally, the EtOAc fraction was subjected to silica gel, C-18, and Sephadex LH-20 column chromatography to yield 8-methoxybutin (4) and leptosidin (5). All the compounds isolated from C. lanceolata inhibited the production of nitric oxide (NO) in LPS-induced BV2 and RAW264.7 cells. In addition, phenylheptatriyne and 4′,7-dimethoxyflavanone reduced the secretion of inflammatory cytokines, tumor necrosis factor alpha (TNF-α), and interleukin (IL)-6. Among them, phenylheptatriyne was significantly downregulated in the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2). Subsequently, phenylheptatriyne also effectively inhibited nuclear factor-kappa B (NF-κB) activation in LPS-stimulated BV2 and RAW264.7 cells. Based on these results, the anti-neuroinflammatory effect of phenylheptatriyne isolated from C. lanceolata was confirmed, which may exert a therapeutic effect in treatment of neuroinflammation-related diseases.

Sign in / Sign up

Export Citation Format

Share Document