scholarly journals INHIBITORY EFFECTS ON TUMOR NECROSIS FACTOR ALPHA AND INTERLEUKIN 12 USING CLOBETASOL PROPIONATE LOADED TEA TREE OIL NANOEMULSION GEL ON ANIMAL MODEL

2018 ◽  
Vol 11 (6) ◽  
pp. 182
Author(s):  
Md Sarfaraz Alam ◽  
Mohamammad Daud Ali ◽  
Md Salahuddin Ansari ◽  
Pankaj Sharma
Keyword(s):  
Clobetasol Propionate ◽  
Interleukin 12 ◽  
Tea Tree Oil ◽  
Necrosis Factor Alpha ◽  
Tea Tree ◽  
Tnf Α ◽  
Nanoemulsion Gel ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Necrosis Factor

Objective: The main objective of our study is to explore anti-inflammatory activity at its molecular level like tumor necrosis factor alpha (TNF-α), interleukin 12 (IL-12) expression, and histopathological study.Methods: As per solubility/miscibility of clobetasol propionate (CP) with tea tree oil (TTO), surfactant and cosurfactant (Smix), and water in a ratio of oil:Smix:water (15:35:50) taken in milliliter for the preparation of nanoemulsion. Induced allergic contact dermatitis (ACD) with dinitrofluorobenzene (DNFB) was used for the study. TNF-α and interleukin 12 (IL-12) were estimated with rabbit antimouse TNF-α and rat antimouse IL-12 antibodies in 1% of bovine serum albumin in phosphate buffer.Results: Topical application of CP loaded nanoemulsion gel inhibits ear inflammation and erythema in DNFB-induced ACD in mice and significantly reduces the intracellular edema and infiltration with inflammatory mediator cells involving of mononuclear cells and neutrophils. CP loaded nanoemulsion gel reduces expression of protein level of TNF-α and IL-12.Conclusion: CP loaded nanoemulsion gel confirmed that anti-inflammatory effects showed more rapidly than the placebo and marketed gel preparation. However, the animals treated with placebo nanoemulsion gel showed a somehow comparable reduction of their inflammation during treatment compared with the marketed gel. This effect may be due to anti-inflammatory effect of TTO. This result suggested that anti-inflammatory activity of placebo nanoemulsion gel may be due to TTO present in nanoemulsion as vehicle.

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.

scholarly journals Hyaluronic Acid-Modified and TPCA-1-Loaded Gold Nanocages Alleviate Inflammation

Pharmaceutics ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 143 ◽  
Author(s):  
Jingnan Zhao
Keyword(s):  
Hyaluronic Acid ◽  
Inflammatory Cells ◽  
Oxygen Species ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Nanogold Particles ◽  
Gold Nanocages ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Necrosis Factor

Gold nanocages (AuNCs) are biocompatible and porous nanogold particles that have been widely used in biomedical fields. In this study, hyaluronic acid (HA) and peptide- modified gold nanocages (HA-AuNCs/T/P) loaded with 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide (TPCA-1) were prepared to investigate their potential for combating inflammation. TPCA-1 was released from AuNCs, intracellularly when HA was hydrolyzed by hyaluronidase. HA-AuNCs/T/P show a much higher intracellular uptake than AuNCs/T/P, and exhibit a much higher efficacy on the suppression of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) than free TPCA-1, suggesting great improvement to the anti-inflammatory efficacy of TPCA-1 through the application of AuNCs. HA-AuNCs/T/P can also reduce the production of reactive oxygen species in inflammatory cells. This study suggests that HA-AuNCs/T/P may be potential agents for anti-inflammatory treatment, and are worthy of further investigation.

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 DNA from Protozoan Parasites Babesia bovis, Trypanosoma cruzi, and T. brucei Is Mitogenic for B Lymphocytes and Stimulates Macrophage Expression of Interleukin-12, Tumor Necrosis Factor Alpha, and Nitric Oxide

2001 ◽  
Vol 69 (4) ◽  
pp. 2162-2171 ◽  
Author(s):  
Lisl K. M. Shoda ◽  
Kimberly A. Kegerreis ◽  
Carlos E. Suarez ◽  
Isabel Roditi ◽  
Ricardo S. Corral ◽  
...  
Keyword(s):  
B Lymphocytes ◽  
Tumor Necrosis ◽  
Babesia Bovis ◽  
Interleukin 12 ◽  
Protozoan Parasites ◽  
Necrosis Factor Alpha ◽  
E Coli ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The activation of innate immune responses by genomic DNA from bacteria and several nonvertebrate organisms represents a novel mechanism of pathogen recognition. We recently demonstrated the CpG-dependent mitogenic activity of DNA from the protozoan parasiteBabesia bovis for bovine B lymphocytes (W. C. Brown, D. M. Estes, S. E. Chantler, K. A. Kegerreis, and C. E. Suarez, Infect. Immun. 66:5423–5432, 1998). However, activation of macrophages by DNA from protozoan parasites has not been demonstrated. The present study was therefore conducted to determine whether DNA from the protozan parasites B. bovis, Trypanosoma cruzi, and T. brucei activates macrophages to secrete inflammatory mediators associated with protective immunity. DNA fromEscherichia coli and all three parasites stimulated B-lymphocyte proliferation and increased macrophage production of interleukin-12 (IL-12), tumor necrosis factor alpha (TNF-α), and nitric oxide (NO). Regulation of IL-12 and NO production occurred at the level of transcription. The amounts of IL-12, TNF-α, and NO induced by E. coli and protozoal DNA were strongly correlated (r 2 > 0.9) with the frequency of CG dinucleotides in the genome, and immunostimulation by DNA occurred in the order E. coli ≥ T. cruzi > T. brucei > B. bovis. Induction of inflammatory mediators by E. coli, T. brucei, and B. bovis DNA was dependent on the presence of unmethylated CpG dinucleotides. However, at high concentrations,E. coli and T. cruzi DNA-mediated macrophage activation was not inhibited following methylation. The recognition of protozoal DNA by B lymphocytes and macrophages may provide an important innate defense mechanism to control parasite replication and promote persistent infection.

scholarly journals Toll-Like Receptor 9 Is Required for Full Host Resistance toMycobacteriumaviumInfection but Plays No Role in Induction of Th1 Responses

2011 ◽  
Vol 79 (4) ◽  
pp. 1638-1646 ◽  
Author(s):  
Natália B. Carvalho ◽  
Fernanda S. Oliveira ◽  
Fernanda V. Durães ◽  
Leonardo A. de Almeida ◽  
Manuela Flórido ◽  
...  
Keyword(s):  
Interleukin 12 ◽  
Toll Like Receptor ◽  
Necrosis Factor Alpha ◽  
Histocompatibility Complex ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Myd88 Signaling ◽  
Necrosis Factor

ABSTRACTTo investigate the role of Toll-like receptor 9 (TLR9) in innate immunity toMycobacteriumavium, TLR9, TLR2, and MyD88 knockout (KO) mice were infected with this bacterium. Bacterial burdens were higher in the spleens, livers, and lungs of infected TLR9 KO mice than in those of C57BL/6 mice, indicating that TLR9 is required for efficient control ofM.aviuminfection. However, TLR9 KO or TLR2 KO spleen cells displayed normalM.avium-induced tumor necrosis factor alpha (TNF-α) and gamma interferon (IFN-γ) responses. This finding was confirmed by determining the number of splenic CD4+T cells producing IFN-γ by flow cytometry. Furthermore, TLR2 and MyD88, but not TLR9, played a major role in interleukin-12 and TNF-α production byM.avium-infected macrophages and dendritic cells (DCs). We also found that major histocompatibility complex class II molecule expression on DCs is regulated by TLR2 and MyD88 signaling but not by TLR9. Finally, lack of TLR9, TLR2, or MyD88 reduced the numbers of macrophages, epithelioid cells, and lymphocytes inM.avium-induced granulomas but only MyD88 deficiency affected the number of liver granulomas. In summary, our data demonstrated that the involvement of TLR9 in the control ofM.aviuminfection is not related to the induction of Th1 responses.

scholarly journals Neutralization of Tumor Necrosis Factor Alpha Suppresses Antigen-Specific Type 1 Cytokine Responses and Reverses the Inhibition of Mycobacterial Survival in Cocultures of Immune Guinea Pig T Lymphocytes and Infected Macrophages

2005 ◽  
Vol 73 (12) ◽  
pp. 8437-8441 ◽  
Author(s):  
Hyosun Cho ◽  
David N. McMurray
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
T Cell Response ◽  
Interleukin 12 ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Neutralization of tumor necrosis factor alpha (TNF-α) significantly down-regulated antigen-induced lymphoproliferation and the expression of interleukin-12 p40 and gamma interferon mRNA and enhanced the viability of intracellular attenuated and virulent mycobacteria in cocultures of immune T cells and macrophages obtained from Mycobacterium bovis BCG-vaccinated guinea pigs. This suggests the crucial role of TNF-α in the activation of a type 1 T-cell response against Mycobacterium tuberculosis infection.

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 The Flavonoid Quercetin Inhibits Proinflammatory Cytokine (Tumor Necrosis Factor Alpha) Gene Expression in Normal Peripheral Blood Mononuclear Cells via Modulation of the NF-κβ System

2006 ◽  
Vol 13 (3) ◽  
pp. 319-328 ◽  
Author(s):  
Madhavan P. Nair ◽  
Supriya Mahajan ◽  
Jessica L. Reynolds ◽  
Ravikumar Aalinkeel ◽  
Harikrishnan Nair ◽  
...  
Keyword(s):  
Gene Expression ◽  
Proinflammatory Cytokine ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Necrosis Factor

ABSTRACT The flavonoids comprise a large class of low-molecular-weight plant metabolites ubiquitously distributed in food plants. These dietary antioxidants exert significant antitumor, antiallergic, and anti-inflammatory effects. The molecular mechanisms of their biological effects remain to be clearly understood. We investigated the anti-inflammatory potentials of a safe, common dietary flavonoid component, quercetin, for its ability to modulate the production and gene expression of the proinflammatory cytokine tumor necrosis factor alpha (TNF-α) by human peripheral blood mononuclear cells (PBMC). Our results showed that quercetin significantly inhibited TNF-α production and gene expression in a dose-dependent manner. Our results provide direct evidence of the anti-inflammatory effects of quercetin by PBMC, which are mediated by the inhibition of the proinflammatory cytokine TNF-α via modulation of NF-κβ1 and Iκβ.

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.

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