scholarly journals Anti-Inflammatory and Anti-Allergic Effects of Saponarin and Its Impact on Signaling Pathways of RAW 264.7, RBL-2H3 and HaCaT Cells

2021 ◽  
Vol 22 (16) ◽  
pp. 8431
Author(s):  
Seon-Young Min ◽  
Che-Hwon Park ◽  
Hye-Won Yu ◽  
Young-Jin Park
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Skin Diseases ◽  
Mitogen Activated Protein Kinase ◽  
Hacat Cells ◽  
Protective Effects ◽  
Tnf Α ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Necrosis Factor

Saponarin{5-hydroxy-2-(4-hydroxyphenyl)-6-[3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]-7-[3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxychromen-4-one}, a flavone found in young green barley leaves, is known to possess antioxidant, antidiabetic, and hepatoprotective effects. In the present study, the anti-inflammatory, anti-allergic, and skin-protective effects of saponarin were investigated to evaluate its usefulness as a functional ingredient in cosmetics. In lipopolysaccharide-induced RAW264.7 (murine macrophage) cells, saponarin (80 μM) significantly inhibited cytokine expression, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, inducible nitric oxide synthase, and cyclooxygenase (COX)-2. Saponarin (80 μM) also inhibited the phosphorylation of extracellular signal-regulated kinase (ERK) and p38 involved in the mitogen-activated protein kinase signaling pathway in RAW264.7 cells. Saponarin (40 μM) significantly inhibited β-hexosaminidase degranulation as well as the phosphorylation of signaling effectors (Syk, phospholipase Cγ1, ERK, JNK, and p38) and the expression of inflammatory mediators (tumor necrosis factor [TNF]-α, IL-4, IL-5, IL-6, IL-13, COX-2, and FcεRIα/γ) in DNP-IgE- and DNP-BSA-stimulated RBL-2H3 (rat basophilic leukemia) cells. In addition, saponarin (100 μM) significantly inhibited the expression of macrophage-derived chemokine, thymus and activation-regulated chemokine, IL-33, thymic stromal lymphopoietin, and the phosphorylation of signaling molecules (ERK, p38 and signal transducer and activator of transcription 1 [STAT1]) in TNF-α- and interferon (IFN)-γ-stimulated HaCaT (human immortalized keratinocyte) cells. Saponarin (100 μM) also significantly induced the expression of hyaluronan synthase-3, aquaporin 3, and cathelicidin antimicrobial peptide (LL-37) in HaCaT cells, which play an important role as skin barriers. Saponarin remarkably inhibited the essential factors involved in the inflammatory and allergic responses of RAW264.7, RBL-2H3, and HaCaT cells, and induced the expression of factors that function as physical and chemical skin barriers in HaCaT cells. Therefore, saponarin could potentially be used to prevent and relieve immune-related skin diseases, including atopic dermatitis.

Anti-inflammatory agents inhibit the induction of leptin by tumor necrosis factor-α

2002 ◽  
Vol 282 (5) ◽  
pp. R1429-R1435 ◽  
Author(s):  
Brian N. Finck ◽  
Rodney W. Johnson
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Kinase Inhibitor ◽  
Mitogen Activated Protein Kinase ◽  
Epididymal Adipose Tissue ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Leptin Expression ◽  
Necrosis Factor

Tumor necrosis factor (TNF)-α stimulates the secretion of the adipocyte-derived hormone leptin. However, the cellular mechanisms by which TNF-α influences leptin production are poorly understood. To examine this issue, epididymal fat pads were isolated from mice and cultured in recombinant murine TNF-α (100 ng/ml). Compared with medium-treated controls, steady-state leptin expression was increased in TNF-α-treated explants. Culture with inhibitors of translation (cycloheximide) or transcription (actinomycin-D) abrogated the induction of leptin following TNF-α. Explants were also cultured in the presence of the anti-inflammatory p38 mitogen-activated protein kinase inhibitor (SB-203580) or PG J2 metabolite [15-deoxy-Δ12,14-PG J2 (PGJ)] and then exposed to TNF-α. Both compounds completely abolished TNF-α-induced increases in leptin production. To test the relevance of this in vivo, mice were pretreated with PGJ and then given TNF-α. PGJ treatment markedly blunted the TNF-α-induced increase in leptin, TNF-α, and interleukin-6 gene expression in epididymal adipose tissue. Collectively, these data indicate that TNF-α acutely activates leptin expression and that anti-inflammatory agents can abrogate TNF-α-induced hyperleptinemia.

scholarly journals EVALUATION OF AQUEOUS FRUIT EXTRACT OF TAMARINDUS INDICA (L) FOR INHIBITION OF TUMOR NECROSIS FACTOR-a AND CYCLO OXYGENASE ENZYMES IN EXPERIMENTAL ANIMAL

2018 ◽  
Vol 11 (3) ◽  
pp. 57 ◽  
Author(s):  
Mohammad Daud Ali ◽  
Atul Kumar Gupta ◽  
Arif Naseer ◽  
Mohd Aamir Mirza ◽  
Sabir Afzal
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Significant Inhibition ◽  
Tamarindus Indica ◽  
Screening Assay ◽  
Standard Drug ◽  
Cox Inhibitor ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Necrosis Factor

 Objective: The main objective of this study was to assess tumor necrosis factor-α (TNF)-α and cyclooxygenase enzymes (COX) inhibition potency of Tamarindus indica Linn. in comparison to standard drug (indomethacin).Methods: Three plants are selected for the studies, namely: Aloe vera (L.), Terminalia chebula Reitz., and T. indica Linn. Estimation of TNF-α in serum (at 1:10 dilution in PBS) was performed using the immunoenzymatic (ELISA) technique. COX inhibitor screening assay kits were used for estimation of COX.Result: All three plant extracts showed a potent significant inhibition of the COX enzyme as compared to the positive control and standard drug when the animal was administered with 400 mg/kg. These studies indicate that the T. indica plant extract showed significant COX inhibition even at low dose. All the extracts were effective anti-inflammatory in nature, however, T. indica extracts at a dose of 400 mg/kg were found to be most potent. It was found to be comparable with that of Indomethacin 10 mg/kg body weight.Conclusion: The anti-inflammatory activity expressed by all the three plants A. vera (L.), T. chebula Reitz., and T. indica L. Among all three plants T. indica (L) was found to be more active against both TNF-α and COX, and it was comparable to standard drug Indomethacin. Need further studies to elucidate the exact secondary metabolite by which these plants express this activity.

scholarly journals Modification of Tumor Necrosis Factor-α and C-C Motif Chemokine Ligand 18 Secretion by Monocytes Derived from Patients with Diabetic Foot Syndrome

Biology ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 3
Author(s):  
Karine O. Galstyan ◽  
Ludmila V. Nedosugova ◽  
Narine S. Martirosian ◽  
Nikita G. Nikiforov ◽  
Natalia V. Elizova ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Diabetic Foot ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Tnf Α ◽  
Inflammatory Activation ◽  
Chemokine Ligand ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Necrosis Factor

Background: This study involves the investigation of spontaneous and induced secretion of the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) and the anti-inflammatory chemokine C-C motif chemokine ligand 18 (CCL18) by monocytes isolated from blood of patients with long-term type 2 diabetes mellitus (T2DM), both with or without foot ulcers. Methods: A total of 121 patients with T2DM (79 without diabetic foot syndrome (DFS) and 42 patients with DFS) were included. Cluster of Differentiation 14 (CD14+) monocytes were isolated from patients’ blood and stimulated by interferon-γ (IFN-γ) and interleukin-4 (IL-4) for induction of pro- and anti-inflammatory monocyte activation, respectively. The concentrations of TNF-α and CCL18 in the culture medium were measured using ELISA on day 1 and day 6 after cell stimulation. Results: We found a correlation between glycated hemoglobin (HbA1c) and stimulated secretion levels of TNF-α (r = 0.726, p = 0.027) and CCL18 (r = –0.949, p = 0.051) in patients with DFS. There was an increase of pro- and anti-inflammatory activation of monocytes in all patients with different durations of DFS (p < 0.05). However, no stimulation of anti-inflammatory activation was detected in patients with DFS lasting more than 6 months (p = 0.033). Conclusions: Our study showed an increase in pro-inflammatory secretion and a decrease in anti-inflammatory secretion by monocytes isolated from blood of patients with T2DM depending on HbA1c levels and duration of the inflammatory process. These findings allow us to assume that monocytes isolated from T2DM patients are characterized by a biased ability to respond towards pro-inflammatory stimulation, contributing to the chronic wound process.

scholarly journals Bikunin Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Induction in Macrophages

2004 ◽  
Vol 11 (6) ◽  
pp. 1140-1147 ◽  
Author(s):  
Hidenori Matsuzaki ◽  
Hiroshi Kobayashi ◽  
Tatsuo Yagyu ◽  
Kiyoshi Wakahara ◽  
Toshiharu Kondo ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Dose Dependent ◽  
Necrosis Factor

ABSTRACT Bikunin, a Kunitz-type protease inhibitor, exhibits anti-inflammatory activity in protection against cancer and inflammation. To investigate the molecular mechanism of this inhibition, we analyzed the effect of bikunin on tumor necrosis factor alpha (TNF-α) production in human peripheral mononuclear cells stimulated by lipopolysaccharide (LPS), an inflammatory inducer. Here, we show the following results. (i) LPS induced TNF-α expression in time- and dose-dependent manners through phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase pathways. (ii) Bikunin inhibits LPS-induced up-regulation of TNF-α protein expression in a dose-dependent manner, reaching 60% inhibition at the highest doses of bikunin tested (5.0 μM). (iii) Inhibition by bikunin of TNF-α induction correlates with the suppressive capacity of ERK1/2, JNK, and p38 signaling pathways, implicating repressions of at least three different signals in the inhibition. (iv) Bikunin blocks the induction of TNF-α target molecules interleukin-1β (IL-1β) and IL-6 proteins. (v) Bikunin is functional in vivo, and this glycoprotein blocks systemic TNF-α release in mice challenged with LPS. (vi) Finally, bikunin can prevent LPS-induced lethality. In conclusion, bikunin significantly inhibits LPS-induced TNF-α production, suggesting a mechanism of anti-inflammation by bikunin through control of cytokine induction during inflammation. Bikunin might be a candidate for the treatment of inflammation, including septic shock.

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 Chemical Composition and Anti-inflammatory Activity of Chamaecyparis obtusa f. formosana Wood Essential Oil from Taiwan

2014 ◽  
Vol 9 (5) ◽  
pp. 1934578X1400900 ◽  
Author(s):  
Tzu-Chao Chien ◽  
Sheng-Fong Lo ◽  
Chen-Lung Ho
Keyword(s):  
Essential Oil ◽  
Tumor Necrosis ◽  
Chamaecyparis Obtusa ◽  
Composition Analysis ◽  
Murine Macrophage ◽  
Tnf Α ◽  
Cellular Signal ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Necrosis Factor

Chamaecyparis obtusa Siebold & Zucc. f. formosana Hayata (Cupressaceae) is one of the treasured conifers in Taiwan. In this study, the wood essential oil of the species was extracted and its anti-inflammatory bioactivities analyzed. The composition analysis of the essential oil yielded a total of 57 compounds with α-terpineol (19.4%), τ-muurolol (16.9%), borneol (16%), and α-cadinol (10.9%) predominating. The anti-inflammatory assays of the essential oil suggest that C. obtusa f. formosana wood oil has no cytotoxicity, and was capable of inhibiting the expressions of tumor necrosis factor (TNF-α), IL-6, IL-1, pro IL-1β, NO, iNOS, and NLRP3 in murine macrophage cells. It was unable, however, to inhibit the expression of COX-2. Further investigation of the effect of the essential oil on the cellular signal transduction indicated that it was capable of inhibiting ERK1/2, JNK1/2 and p38; it also showed excellent inhibition against ROS. Thus, the overall results indicated that C. obtusa f. formosana wood oil had very good anti-inflammatory efficacies.

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.

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