scholarly journals Caffeic Acid Phenethyl Ester: Consequences of Its Hydrophobicity in the Oxidative Functions and Cytokine Release by Leukocytes

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Luana Chiquetto Paracatu ◽  
Carolina Maria Quinello Gomes Faria ◽  
Camila Quinello ◽  
Camila Rennó ◽  
Patricia Palmeira ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Caffeic Acid ◽  
Superoxide Anion ◽  
Hypochlorous Acid ◽  
Inflammatory Diseases ◽  
Biological Effects ◽  
Caffeic Acid Phenethyl Ester ◽  
Nadph Oxidases ◽  
Tnf Α ◽  
Anti Inflammatory

Numerous anti-inflammatory properties have been attributed to caffeic acid phenethyl ester (CAPE), an active component of propolis. NADPH oxidases are multienzymatic complexes involved in many inflammatory diseases. Here, we studied the importance of the CAPE hydrophobicity on cell-free antioxidant capacity, inhibition of the NADPH oxidase and hypochlorous acid production, and release of TNF-α and IL-10 by activated leukocytes. The comparison was made with the related, but less hydrophobic, caffeic and chlorogenic acids. Cell-free studies such as superoxide anion scavenging assay, triene degradation, and anodic peak potential(Epa)measurements showed that the alterations in the hydrophobicity did not provoke significant changes in the oxidation potential and antiradical potency of the tested compounds. However, only CAPE was able to inhibit the production of superoxide anion by activated leukocytes. The inhibition of the NADPH oxidase resulted in the blockage of production of hypochlorous acid. Similarly, CAPE was the more effective inhibitor of the release of TNF-α and IL-10 byStaphylococcus aureusstimulated cells. In conclusion, the presence of the catechol moiety and the higher hydrophobicity were essential for the biological effects. Considering the involvement of NADPH oxidases in the genesis and progression of inflammatory diseases, CAPE should be considered as a promising anti-inflammatory drug.

scholarly journals Caffeic Acid Phenethyl Ester Attenuates Gingival Tissue Inflammation in Experimental Periodontitis

2021 ◽  
Author(s):  
Esra DEMİR ◽  
Feyza Otan ÖZDEN ◽  
Bahattin AVCI
Keyword(s):  
Caffeic Acid ◽  
Alveolar Bone ◽  
Caffeic Acid Phenethyl Ester ◽  
Gingival Tissue ◽  
Dependent Manner ◽  
Tnf Α ◽  
Significant Difference ◽  
Experimental Periodontitis ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Abstract Caffeic acid phenethyl ester (CAPE) is an active component of propolis extracts and has anti-inflammatory, antioxidant, immunomodulatory activities. This study aims to investigate the anti-inflammatory effect of two different dosages of CAPE on lipopolysaccharide-induced experimental periodontitis (EP). Forty Sprague Dawley rats were randomly divided into four groups: control, EP, EP treated with 5 µmol/kg/day of CAPE (EP + CAPE 5), and EP treated with 10 µmol/kg/day of CAPE (EP + CAPE 10). Followed by the EP, CAPE was administered intraperitoneally to the EP + CAPE groups for 28 days. Samples were investigated biochemically using an enzyme linked immunoassay (ELISA) kit and alveolar bone loss was measured morphometrically. In both of the CAPE groups, the levels of IL-1β and TNF-α in the gingiva were significantly lower than those in the EP group (p < 0.001). The decrease in tissue levels of TNF-α was greater in the EP + CAPE 10 group than in the EP + CAPE 5 group in a dose-dependent manner. Serum analysis of the cytokines showed no significant difference between the groups. Within the limits of this study, CAPE showed its anti-inflammatory effect by reducing pro-inflammatory cytokines in gingiva and is claimed to be a novel agent in improving the results of periodontal therapy without any known side effects.

Abstract 035: Cholinergic Agonists Protect from the Development of Hypertension during Chronic Inflammatory Disease

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Keisa W Mathis
Keyword(s):  
Protein Expression ◽  
Lupus Erythematosus ◽  
Inflammatory Diseases ◽  
Autoimmune Disorder ◽  
Chronic Inflammatory Disease ◽  
Cholinergic Agonists ◽  
Inflammatory Pathway ◽  
Genetic Mouse Model ◽  
Tnf Α ◽  
Anti Inflammatory

Systemic lupus erythematosus (SLE) is an autoimmune disorder with prevalent hypertension. Previous studies using a genetic mouse model of SLE (NZBWF1) suggest chronic inflammation is an important contributor to SLE hypertension. A novel neuroimmune pathway involving the α7 subunit of the nicotinic acetylcholine receptor (α7nAChR) suppresses splenic cytokine release and reduces systemic inflammation upon stimulation. To test whether activation of this ‘cholinergic anti-inflammatory pathway’ at the level of the α7nAChR attenuates the development of hypertension during SLE, female SLE and control (NZW) mice were infused with nicotine hydrogen tartrate salt (2 mg/kg/day, SC) or saline for 7 days. Nicotine-treated SLE mice had lower splenic protein expression of TNF-α and IL-6 (normalized to β-actin) relative to saline-treated SLE mice (1.09±0.06 vs. 1.37±0.06 and 0.36±0.04 vs. 0.55±0.10; all p<0.05), suggesting efficacy of the therapy. Mean arterial pressure (MAP; mmHg) was increased in SLE mice compared to controls (140±4 vs. 114±2; p<0.001). Nicotine prevented the rise in MAP in SLE mice (129±4; p=0.022), but not controls (121±3). This protection from hypertension coincided with a 46±5% lower renal cortical TNF-α in nicotine-treated SLE mice compared to saline-treated SLE mice (0.39±0.04 vs. 0.73±0.18), which is important because it has been previously shown that renal TNF-α plays a mechanistic role in the development of hypertension during SLE. Because nicotine acts on both ganglionic and peripheral cholinergic receptors, in a subsequent study mice were administered the selective α7nAChR agonist, PNU-282987 (0.38 mg/kg/day, IP), or vehicle for 28 days. PNU-282987-treated SLE mice had lower splenic protein expression of TNF-α and IL-6 relative to saline-treated SLE mice (0.33±0.01 vs. 0.54±0.03 and 0.40±0.08 vs. 0.86±0.05; all p<0.05). MAP was increased in SLE mice compared to controls (138±2 vs. 122±5). PNU-282987 prevented the rise in MAP in SLE mice (128±4), but not controls (125±5). These data suggest the anti-inflammatory effects of cholinergic agonists may protect from SLE hypertension and that the cholinergic anti-inflammatory pathway may be an important target in hypertensive patients with chronic inflammatory diseases.

scholarly journals NOx-, IL-1β-, TNF-α-, and IL-6-Inhibiting Effects and Trypanocidal Activity of Banana (Musa acuminata) Bracts and Flowers: UPLC-HRESI-MS Detection of Phenylpropanoid Sucrose Esters

Molecules ◽  
2019 ◽  
Vol 24 (24) ◽  
pp. 4564
Author(s):  
Louis P. Sandjo ◽  
Marcus V. P. dos Santos Nascimento ◽  
Milene de H. Moraes ◽  
Luiza Manaut Rodrigues ◽  
Eduardo M. Dalmarco ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Musa Acuminata ◽  
Sucrose Esters ◽  
Food Ingredient ◽  
Trypanocidal Activity ◽  
Traditional Remedy ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Anti Inflammatory ◽  
Inflammatory Action

Banana inflorescences are a byproduct of banana cultivation consumed in various regions of Brazil as a non-conventional food. This byproduct represents an alternative food supply that can contribute to the resolution of nutritional problems and hunger. This product is also used in Asia as a traditional remedy for the treatment of various illnesses such as bronchitis and dysentery. However, there is a lack of chemical and pharmacological data to support its consumption as a functional food. Therefore, this work aimed to study the anti-inflammatory action of Musa acuminata blossom by quantifying the cytokine levels (NOx, IL-1β, TNF-α, and IL-6) in peritoneal neutrophils, and to study its antiparasitic activities using the intracellular forms of T. cruzi, L. amazonensis, and L. infantum. This work also aimed to establish the chemical profile of the inflorescence using UPLC-ESI-MS analysis. Flowers and the crude bract extracts were partitioned in dichloromethane and n-butanol to afford four fractions (FDCM, FNBU, BDCM, and BNBU). FDCM showed moderate trypanocidal activity and promising anti-inflammatory properties by inhibiting IL-1β, TNF-α, and IL-6. BDCM significantly inhibited the secretion of TNF-α, while BNBU was active against IL-6 and NOx. LCMS data of these fractions revealed an unprecedented presence of arylpropanoid sucroses alongside flavonoids, triterpenes, benzofurans, stilbenes, and iridoids. The obtained results revealed that banana inflorescences could be used as an anti-inflammatory food ingredient to control inflammatory diseases.

scholarly journals Canscora lucidissima, a Chinese folk medicine, exerts anti-inflammatory activities by inhibiting the phosphorylation of ERK1/2 in LPS-activated macrophages

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Qiao-ling Fei ◽  
Xiao-yu Zhang ◽  
Rui-juan Qi ◽  
Yun-feng Huang ◽  
Yi-xin Han ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Southern China ◽  
Raw 264.7 Cells ◽  
Luciferase Reporter ◽  
Effective Treatment Option ◽  
Proinflammatory Mediators ◽  
Inflammatory Models ◽  
Inflammatory Mechanism ◽  
Tnf Α ◽  
Anti Inflammatory

Abstract Background Canscora lucidissima (Levl. & Vaniot) Hand.-Mazz. (C. lucidissima), mainly distributed in southern China, has been shown to be effective in the treatment of inflammatory diseases. However, the underlying mechanism of its anti-inflammatory effect is not fully understood. Methods In this study, we investigated the anti-inflammatory mechanism of ethanol extract of C. lucidissima (Cl-EE) in lipopolysaccharide (LPS)-induced inflammatory models. ELISA, real-time PCR, Western blot and luciferase reporter assay were used for the experiments in vitro, and ICR mouse endotoxemia model was used for in vivo test. Results Our data showed that Cl-EE reduced the production of NO by down-regulating the mRNA and protein expression of inducible nitric oxide synthase (iNOS) in LPS-activated RAW 264.7 cells. Meanwhile, it potently decreased other proinflammatory mediators, such as TNF-α, IL-6, MCP-1 and IL-1β at the transcriptional and translational levels. Further study indicated that Cl-EE did not affect NF-κB signaling pathway but significantly suppressed the phosphorylation of ERK1/2, rather than JNK or p38. In a LPS-induced endotoxemia mouse model, a single intraperitoneal injection of Cl-EE (75–300 mg/kg) could lower circulatory TNF-α, IL-6 and MCP-1 levels. Conclusions Collectively, our results indicated that Cl-EE suppressed the phosphorylation level of ERK1/2 thus reducing the transcription and translation of inflammatory genes, thereby exerted anti-inflammatory activity. This study reveals the anti-inflammatory mechanism of C. lucidissima and may provide an effective treatment option for a variety of inflammatory diseases.

Antinociceptive and Anti-Inflammatory Activities ofCuscuta chinensisSeeds in Mice

2014 ◽  
Vol 42 (01) ◽  
pp. 223-242 ◽  
Author(s):  
Jung-Chun Liao ◽  
Wen-Te Chang ◽  
Meng-Shiou Lee ◽  
Yung-Jia Chiu ◽  
Wei-Kai Chao ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Inflammatory Diseases ◽  
Antinociceptive Effect ◽  
Inflammatory Mechanism ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Highly Correlated ◽  
Cuscuta Chinensis ◽  
Inflammatory Effect

The seeds of Cuscuta chinensis, Cuscutae Semen, are commonly used as a medicinal material for treating the aching and weakness of the loins and knees, tonifying the defects of the liver and the kidney, and treating the diarrhea due to hypofunction of the kidney and the spleen. Since aching and inflammation are highly correlated with such diseases, the aim of this study is to investigate the possible antinociceptive and anti-inflammatory mechanisms of the seeds of C. chinensis. The antinociceptive effect of the seeds of C. chinensis was evaluated via the acetic acid-induced writhing response and formalin-induced paw licking methods. The anti-inflammatory effect was evaluated via the λ-carrageenan induced mouse paw edema method. The results found that 100 and 500 mg/kg of the methanol extract of the seeds of C. chinensis( CCMeOH) significantly decreased (p < 0.01 and p < 0.001, respectively) the writhing response in the acetic acid assay. Additionally, 20–500 mg/kg of CCMeOHsignificantly decreased licking time at the early (20 and 100 mg/kg, p < 0.001) and late phases (100 mg/kg, p < 0.01; 500 mg/kg, p < 0.001) of the formalin test, respectively. Furthermore, CCMeOH(100 and 500 mg/kg) significantly decreased (p < 0.01 and p < 0.001, respectively) edema paw volume four hours after λ-carrageenan had been injected. The results in the following study also revealed that the anti-inflammatory mechanism of CCMeOHmay be due to declined levels of NO and MDA in the edema paw by increasing the activities of SOD, GPx and GRd in the liver. In addition, CCMeOHalso decreased IL-1β, IL-6, NF-κB, TNF-α, and COX-2 levels. This is the first study to demonstrate the possible mechanisms for the antinociceptive and anti-inflammatory effects of CCMeOHin vivo. Thus, it provides evidence for the treatment of Cuscutae Semen in inflammatory diseases.

scholarly journals Analgesic and Anti-Inflammatory Activities of Methanol Extract ofFicus pumilaL. in Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Chi-Ren Liao ◽  
Chun-Pin Kao ◽  
Wen-Huang Peng ◽  
Yuan-Shiun Chang ◽  
Shang-Chih Lai ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Methanol Extract ◽  
Inflammatory Diseases ◽  
Paw Edema ◽  
Tissue Destruction ◽  
Hplc Fingerprint ◽  
Analgesic Effects ◽  
Inflammatory Mechanism ◽  
Tnf Α ◽  
Anti Inflammatory

This study investigated possible analgesic and anti-inflammatory mechanisms of the methanol extract ofFicus pumila(FPMeOH). Analgesic effects were evaluated in two models including acetic acid-induced writhing response and formalin-induced paw licking. The results showedFPMeOHdecreased writhing response in the acetic acid assay and licking time in the formalin test. The anti-inflammatory effect was evaluated by λ-carrageenan-induced mouse paw edema and histopathological analyses.FPMeOHsignificantly decreased the volume of paw edema induced by λ-carrageenan. Histopathologically,FPMeOHabated the level of tissue destruction and swelling of the edema paws. This study indicated anti-inflammatory mechanism ofFPMeOHmay be due to declined levels of NO and MDA in the edema paw through increasing the activities of SOD, GPx, and GRd in the liver. Additionally,FPMeOHalso decreased the level of inflammatory mediators such as IL-1β, TNF-α, and COX-2. HPLC fingerprint was established and the contents of three active ingredients, rutin, luteolin, and apigenin, were quantitatively determined. This study provided evidence for the classical treatment ofFicus pumilain inflammatory diseases.

Fermentation Improves Anti-Inflammatory Effect of Sipjeondaebotang on LPS-Stimulated RAW 264.7 Cells

2012 ◽  
Vol 40 (04) ◽  
pp. 813-831 ◽  
Author(s):  
You-Chang Oh ◽  
Won-Kyung Cho ◽  
Yun Hee Jeong ◽  
Ga Young Im ◽  
Min Cheol Yang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Mediators ◽  
High Performance ◽  
Biological Effects ◽  
Inhibitory Effect ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Tnf Α ◽  
Cox 2 ◽  
Anti Inflammatory

Sipjeondaebotang (SJ) has been used as a traditional drug in east-Asian countries. In this study, to provide insight into the biological effects of SJ and SJ fermented by Lactobacillus, we investigated their effects on lipopolysaccharide (LPS)-mediated inflammation in macrophages. The investigation was focused on whether SJ and fermented SJ could inhibit the production of pro-inflammatory mediators such as prostaglandin (PG) E2 and nitric oxide (NO) as well as the expressions of cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-α, mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-κB in LPS-stimulated RAW 264.7 cells. We found that SJ modestly inhibited LPS-induced PGE2, NO and TNF-α production as well as the expressions of COX-2 and iNOS. Interestingly, fermentation significantly increased its inhibitory effect on the expression of all pro-inflammatory mediators. Furthermore, fermented SJ exhibited increased inhibition of p38 MAPK and c-Jun NH2-terminal kinase (JNK) MAPK phosphorylation as well as NF-κB p65 translocation by reduced IκBα degradation compared with either untreated controls or unfermented SJ. High performance liquid chromatography (HPLC) analysis showed fermentation by Lactobacillus increases liquiritigenin and cinnamyl alcohol contained in SJ, which are known for their anti-inflammatory activities. Finally, SJ fermented by Lactobacillus exerted potent anti-inflammatory activity by inhibiting MAPK and NF-κB signaling in RAW 264.7 cells.

scholarly journals Screening of an anti-inflammatory peptide from Hydrophis cyanocinctus and analysis of its activities and mechanism in DSS-induced acute colitis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Zengjie Zheng ◽  
Hailong Jiang ◽  
Yan Huang ◽  
Jie Wang ◽  
Lei Qiu ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Activity Index ◽  
Tumor Necrosis Factor Receptor ◽  
Disease Activity Index ◽  
Acute Colitis ◽  
Surface Plasmon Resonance Analysis ◽  
Tnf Α ◽  
Anti Inflammatory

Abstract Snake has been used for centuries as a traditional Chinese medicine, especially for therapeutic treatment for inflammatory diseases; however, its mechanisms of action and active constituents remain controversial. In our study, a tumor necrosis factor receptor 1 (TNFR1) selective binding peptide, Hydrostatin-SN1 (H-SN1), which was screened from a Hydrophis cyanocinctus venom gland T7 phage display library, was shown to exhibit significant anti-inflammatory activity in vitro and in vivo. As a TNFR1 antagonist, it reduced cytotoxicity mediated by TNF-α in L929 fibroblasts and effectively inhibited the combination between TNF-α with TNFR1 in surface plasmon resonance analysis. H-SN1 was also shown to suppress TNFR1–associated signaling pathways as it minimized TNF-α-induced NF-кB and MAPK activation in HEK293 embryonic kidney and HT29 adenocarcinoma cell lines. We next determined the effect of H-SN1 in vivo using a murine model of acute colitis induced by dextran sodium sulfate, demonstrating that H-SN1 lowered the clinical parameters of acute colitis including the disease activity index and histologic scores. H-SN1 also inhibited TNF/TNFR1 downstream targets at both mRNA and protein levels. These results indicate that H-SN1 might represent a suitable candidate for use in the treatment of TNF-α-associated inflammatory diseases such as inflammatory bowel diseases.

scholarly journals Complex responses to inflammatory oxidants by the probiotic bacterium Lactobacillus reuteri

2019 ◽  
Author(s):  
Poulami Basu Thakur ◽  
Abagail R. Long ◽  
Benjamin J. Nelson ◽  
Ranjit Kumar ◽  
Alexander F. Rosenberg ◽  
...  
Keyword(s):  
Immune System ◽  
Hypochlorous Acid ◽  
Lactobacillus Reuteri ◽  
Inflammatory Diseases ◽  
Small Heat Shock Protein ◽  
Probiotic Bacterium ◽  
Transcriptomic Response ◽  
E Coli ◽  
Anti Inflammatory ◽  
Associated Species

ABSTRACTInflammatory diseases of the gut are associated with increased intestinal oxygen concentrations and high levels of inflammatory oxidants, including hydrogen peroxide (H2O2) and hypochlorous acid (HOCl), which are antimicrobial compounds produced by the innate immune system. This contributes to dysbiotic changes in the gut microbiome, including increased populations of pro-inflammatory enterobacteria (Escherichia coli and related species) and decreased levels of health-associated anaerobic Firmicutes and Bacteroidetes. The pathways for H2O2 and HOCl resistance in E. coli have been well-studied, but little is known about how commensal and probiotic bacteria respond to inflammatory oxidants. In this work, we have characterized the transcriptomic response of the anti-inflammatory, gut-colonizing Gram-positive probiotic Lactobacillus reuteri to both H2O2 and HOCl. L. reuteri mounts distinct responses to each of these stressors, and both gene expression and survival were strongly affected by the presence or absence of oxygen. Oxidative stress response in L. reuteri required several factors not found in enterobacteria, including the small heat shock protein Lo18, polyphosphate kinase 2, and RsiR, an L. reuteri-specific regulator of anti-inflammatory mechanisms. These results raise the intriguing possibility of developing treatments for inflammatory gut diseases that could sensitize pro-inflammatory enterobacteria to killing by the immune system while sparing anti-inflammatory, health-associated species.IMPORTANCEIt is becoming increasingly clear that effective treatment of inflammatory gut diseases will require modulation of the gut microbiota. Preventing pro-inflammatory bacteria from blooming while also preserving anti-inflammatory and commensal species is a considerable challenge, but our results suggest that it may be possible to take advantage of differences in the way different species of gut bacteria resist inflammatory oxidants to accomplish this goal.

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