Cell Exudation Research Articles

Jasmonic acid enhances the resistance of potato plants in vitro to salt stress

The protective effect of jasmonic acid (JA) was evaluated under stress (100 mM NaCl) condition. The investigations were carried on potato plants (Solanum tuberosum L.) of the mid-season variety Lugovskoy. Plant-regenerants were grafted and cultured in test tubes on modified Murashige-Skoog agar medium in the absence (control) or in the presence of JA at concentrations of 0.001; 0.1 and 10 M under optimal growing conditions or with the addition of NaCl. After 28 days of cultivation, growth (length of stem and root, number of tiers and leaves, plant mass) and physiological (proline content and photosynthetic pigments, determination of the osmotic potential of cell exudate) of the plants were assessed. For the first time it has been shown that jasmonic acid (0.1 and 10 M) manifests a pronounced protective effect on potato plants under salt stress condition. The protective effect based on the partial removal of the salt negative effect on the main photosynthetic pigments and the maintenance of the osmotic status of cell contents during salinization.

Jasmonic Acid Enhances the Potato Plant Resistance to the Salt Stress in Vitro

The protective effect of jasmonic acid (JA) was evaluated under the stress conditions (100 mM NaCl). The potato plants Solanum tuberosum L, mid-season variety Lugovskoy, were used in the experiments. The plant-regenerants were grafted and grown in test tubes on the modified Murashige and Skoog agar medium in the absence (control) or presence of JA at concentrations of 0.001, 0.1, and 10 μM under the optimal conditions or with addition of NaCl. After 28 days of cultivation, the growth (stem and root lengths, tier and leaf numbers, and plant mass) and physiological (proline and photosynthetic pigment contents and teh osmotic potential of cell exudate) characteristics of the plants were assessed. Jasmonic acid (0.1 and 10 μM) has been demonstrated to display a pronounced protective effect on potato plants under the salt stress condition. JA abolished partially the negative salt effect on the main photosynthetic pigments and maintained the cell osmotic status during salinization.

The Ecto-5'-Nucleotidase/CD73 Inhibitor, α,β-Methylene Adenosine 5'-Diphosphate, Exacerbates Carrageenan-Induced Pleurisy in Rat.

The ecto-5’-nucleotidase (ecto-5’NT/CD73) represents a crucial enzyme for endogenous adenosine generation. Several findings have shown that CD73 plays an important role in regulating vascular permeability and immune cell function. Adenosine 5’-(α,β-methylene)diphosphate (APCP) is a CD73 inhibitor, widely used as pharmacological tool to investigate the role of CD73/adenosine pathway in several in vitro and in vivo models, although it has been also shown to inhibit other ectoenzymes involved in adenosinergic pathway. Here, we evaluated the effect of APCP in the development of inflammation in carrageenan-induced pleurisy model. We found that treatment with APCP (400 µg/rat) significantly increased cell accumulation, exudate formation, and pro-inflammatory cytokine content into the pleural cavity in the acute phase (4 h) of inflammation, with no differences in the sub-acute phase (72 h) except for the regulation of monocyte chemotactic protein-1 levels. In addition, cells collected by pleural lavage fluids of APCP-treated rats, 4 h following carrageenan injection, showed increased ability to migrate in vitro, both in presence and in absence of N-formyl-L-methionyl-L-leucyl-L-phenylalanine as chemotactic stimulus, compared to cells obtained by control rats. Our results demonstrate that APCP exacerbates the early phase of carrageenan-induced pleurisy by controlling pleural effusion and polymorphonuclear migration in vivo and ex vivo. This effect is likely dependent upon CD73 inhibition, although an inhibitory effect of other ectoenzymes cannot be ruled out.

Development of a Pseudomonas syringae-Arabidopsis Suspension Cell Infection System for Investigating Host Metabolite-Dependent Regulation of Type III Secretion and Pattern-Triggered Immunity.

The importance of pattern-triggered immunity (PTI) in plant defense has been clearly established through genetic studies of mutants lacking functional pattern recognition receptors (PRRs) and signaling components downstream of PRR activation. Despite extensive knowledge of PRR-mediated signaling responses to pathogen-associated molecular patterns (PAMPs), little is known about which of these responses, if any, are directly responsible for limiting bacterial growth. In this work, we established a protocol for coculturing the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 and Arabidopsis suspension cells. The system closely mirrors infection processes that occur in leaves, with bacteria relying on the type III secretion system (T3SS) for maximal growth and PAMP-induced plant defenses effectively limiting bacterial growth. To demonstrate the utility of this system, we investigated the molecular basis of PAMP-induced growth inhibition and discovered that T3SS-associated genes are inhibited when DC3000 is cocultured with PAMP-treated plant suspension cells. To determine the underlying mechanism of decreased T3SS gene expression, we performed metabolomics and biochemical analyses of suspension cell exudates and identified 14 metabolites that significantly increased or decreased following PAMP treatment. Citric acid, a known inducer of T3SS gene expression in DC3000, was among several organic acids decreased in exudates from PAMP-treated plant cells. Exogenous addition of citric acid increased T3SS gene expression and partially recovered growth of DC3000 in the presence of PAMP-treated cells, indicating that a portion of PAMP-induced defense in this system is decreased extracellular release of this metabolite. We envision that the well-defined infection conditions of this coculture system will be valuable for quantitative studies of type III effector delivery by P. syringae. Furthermore, this system provides a unique 'top-down' approach to unravel the molecular basis of PTI against P. syringae.

Reflux Nephropathy and Vesico-Ureteric Reflux in Children - Radionuclide Technique

Reflux nephropathy is defined as 'renal scarring' associated with vesica-ureteral reflux (VUR) and consists of calyceal clubbing or deformity with overlying corticomedullary scarring. The older terms chronic pyelonephritis and chronic atrophic pyelonephritis should be strictly defined as a persistent or recurrent bacterial infection of the kidney involving the renal parenchyma and the pelvi-calyceal system with exudation of inflammatory cells.

Erlotinib Protects LPS-Induced Acute Lung Injury in Mice by Inhibiting EGFR/TLR4 Signaling Pathway.

Epidermal growth factor receptor (EGFR) has been reported to initiate the inflammatory response, but its activation in lipopolysaccharide (LPS)-induced murine model of acute lung injury (ALI) remains unclear. In this study, we investigated the role of EGFR in the LPS-induced murine model of ALI and explored whether its inhibitor erlotinib could affect the progression of lung injury. We first detected the phosphorylated EGFR (p-EGFR)/EGFR ratio at different time points after LPS stimulation, and then different concentrations of erlotinib were used to treat mice at 1 h before LPS stimulation and collected samples at the time point of the highest p-EGFR/EGFR ratio. Lung injury indicators were detected and compared among groups. EGFR and toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signal transduction factors, including p-EGFR, p-AKT, p-ERK1/2, p-p65, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β), were measured with western blot. We found that the mice challenged with LPS suffered from the most serious lung injury at 24 h after LPS stimulation when the p-EGFR/EGFR ratio was relatively the highest. Erlotinib significantly diminished LPS-induced exudation of total cells, neutrophils, and proteins in BALF. Both the ELISA and western blot results showed that erlotinib attenuated the expression of TNF-α and IL-1β in LPS-induced ALI in mice. Inhibition of EGFR by erlotinib downregulated the expression of p-p65 protein level as well as blocked the activation of AKT and ERK1/2 signaling pathway. Taken together, erlotinib alleviated the LPS-induced ALI in a dose-dependent manner by suppressing EGFR activation and downregulating the NF-κB-mediated secretion of proinflammatory cytokines.

Aloperine suppresses allergic airway inflammation through NF-κB, MAPK, and Nrf2/HO-1 signaling pathways in mice

To explore the effects of aloperine (ALO) on allergic airway inflammation, we investigated whether its mechanism is related with NF-κB, MAPK, and Nrf2/HO-1 signaling pathways. Histochemical staining and inflammatory cell count were used to observe lung histopathological changes in mice. ELISA was used to detect the content of inflammatory cytokines and IgE in the mouse bronchoalveolar lavage fluid (BALF). Airway hyperresponsiveness (AHR) to inhale methacholine was measured by the plethysmography in conscious mice. Immunohistochemical method was used to detect the expression levels of Nrf2 and HO-1 in lung tissues. The key proteins of MAPK, NF-κB, and Nrf2/HO-1 in lung tissues were quantitatively analyzed by Western blot. Finally, the in vitro effect of ALO on the production of pro-inflammatory mediators and cytokines by lipopolysaccharide-stimulated RAW 264.7 cells was also evaluated. In the ovalbumin (OVA)-induced asthma mouse model, ALO reduced the exudation and infiltration of inflammatory cells and suppressed goblet cell hyperplasia. ALO-treated asthmatic mice also decreased the protein levels of interleukin (IL)-4, IL-5, IL-13, IFN-γ, and IgE in BALF and attenuated AHR. Furthermore, ALO inhibited the expression of key proteins of MAPK and NF-κB pathways, and increased the expression of Nrf2/HO-1 in OVA-challenged mice. Additional in vitro study has shown that ALO abrogates the macrophage production of inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-α, IL-6, and IL-1β. Taken together, ALO attenuated allergic airway inflammation through regulating NF-κB, MAPK, and Nrf2/HO-1 signaling pathways. The results suggest the utility of ALO as an anti-inflammatory agent for the treatment of asthma.

Transplantation of Endothelial Progenitor Cells Attenuates Lipopolysaccharide-Induced Lung Injury via Inhibiting the Inflammatory Secretion of Neutrophils in Rats

BackgroundEndothelial progenitor cells (EPCs) are special types of stem cells and are a potential novel therapeutic approach in acute lung injury (ALI). Transplantation of EPCs can ameliorate the inflammatory state by reducing adhesion and exudation of inflammatory cells. However, the mechanism underlying the effect of EPCs on inflammatory response modulation remains unclear. The aim of the present study was to investigate the effect of EPCs on the modulation of neutrophils in vitro and in vivo. Materials and MethodsEPCs were cocultured with neutrophils after lipopolysaccharide stimulation in vitro or transplanted into ALI rats, and neutrophil inflammatory mediators including tumor necrosis factor-α, interleukin-1β, neutrophil elastase, myeloperoxidase and matrix metalloproteinases-9 were detected by enzyme-linked immunosorbent assay, an myeloperoxidase detection kits, reverse transcription-polymerase chain reaction and western blotting. ResultsThe results showed that EPCs significantly downregulated the expression of inflammatory mediators when cocultured with neutrophils in vitro or in vivo. ConclusionsThese findings demonstrated that EPCs contributed to lung injury in ALI rats by downregulating neutrophil inflammatory mediators.

Role of neutrophils in CVB3 infection and viral myocarditis

Coxsackievirus B3 (CVB3) is a globally prevalent enterovirus of the Picornaviridae family that is frequently associated with viral myocarditis (VM). Neutrophils, as first responders, may be key cells in determining viral disease outcomes; however, neutrophils have been poorly studied with respect to viral infection. Although neutrophils have been ascribed a relevant role in early cardiac inflammation, their precise role in CVB3 infection has not yet been evaluated. In this study, we aimed to determine if the interaction between human neutrophils and CVB3 could lead to viral replication and/or modulation of neutrophil survival and biological functions, and whether neutrophil depletion in a murine model has a beneficial or harmful effect on CVB3 infection. Our results show that CVB3 interacted with but did not replicate in human neutrophils. Neutrophils recognized CVB3 mainly through endosomal TLR-8, and infection triggered NFκB activation. Virus internalization resulted in increased cell survival, up-regulation of CD11b, enhanced adhesion to fibrinogen and fibronectin, and the secretion of IL-6, IL-1β, TNF-α, and IL-8. Supernatants from infected neutrophils exerted chemotactic activity partly mediated by IL-8. The infected neutrophils released myeloperoxidase and triggered neutrophil extracellular trap formation in the presence of TNF-α. In mice infected with CVB3, viral RNA was detected in neutrophils as well as in mononuclear cells. After neutrophil depletion, mice showed reduced VM reflected by a reduction in viral titers, cell exudates, and CCL-2 mRNA levels, as well as the abrogation of reactive cardiomyocyte hypertrophy. Our results indicate that neutrophils have relevant direct and indirect roles in the pathogenesis of CVB3-induced VM.

Effect of Different Concentrations of Moxa-smoke on Lung Function and TNF-α and IL-1 β Levels in Serum and Lung Tissues in Normal Rats

To study the effect of moxa-smoke inhaling on the respiratory system, so as to provide experimental data and theoretical basis for evaluating the safety of moxa-smoke inhaling during moxibustion treatment. A total of 48 SD rats were randomized into control, low, medium and high moxa-smoke-concentration groups (n＝12 in each group). The low, medium and high concentrations of smoke were controlled in (0.11±0.05) mg/m3, (0.23±0.05) mg/m3 and (0.53±0.05) mg/m3 respectively in each of 3 glass boxes (with reference to the level of PM 2.5). The smoking was conducted 4 hours each time, twice a day for 100 days. The normal group did not receive any moxa-smoke inhaling. The histopathological changes of lung and bronchial tissues were detected by H．E. stainning, and the contents of TNF-α and IL-1 β of plasma, bronchoalveolar la-vage fluid (BALF) and lung tissue detected by ELISA. The levels of forced vital capacity (FVC), forced expiratory volume (FEV), FEV 0.3/FVC (0.3＝ the 0.3rd second), maximal mid-expiratory flow rate(MMEF), peak expiratory flow(PEF) were detected by animal pulmonary function analysis system. After 100 days' moxa-smoke inhaling, the contents of TNF-α in the plasma, BALF and lung tissues and IL-1 β in the lung tissue of the low, medium and high concentration moxa-smoke groups, and IL-1 β in the plasma and BALF of the medium and high concentration groups were significantly increased relevant to the control group (P<0.05, P<0.01). H．E. stain showed various inflammatory changes in the lungs and trachea tissues, including obvious fusion of pulmonary alveoli, lymphocyte infiltration, increase of capillary permeability, red blood cell exudation, etc. in the high concentration group, these situations were milder in the medium concentration group and were not obvious in the low concentration group. Compared with the control group, there were no significant changes in the FVC, FEV, FEV 0.3/FVC, MMEF and PEF of lung function in the three concentration groups (P> 0.05)．. Long term inhalation of high concentration of moxa-smoke may lead to inflammatory injury in the lung and bronchial tissues but has no significant effect on the respiratory function in rats. Nevertheless, a good air-ventilation during moxibustion in a treatment room is necessary.

Omega-3-carboxylic acids provide efficacious anti-inflammatory activity in models of crystal-mediated inflammation

This study assesses the efficacy and exposure–response relationship of omega-3-carboxylic acids (OM-3 CA) in models of crystal-based inflammation. Human THP-1 macrophages and primary peripheral blood mononuclear cells exposed to multiple inflammatory crystal types were used to determine the anti-inflammatory potential of omega-3 (OM-3) fatty acids in vitro. Anti-inflammatory effects of OM-3 CA in vivo were tested in rat monosodium urate (MSU) crystal air pouch and rat knee intra-articular MSU injection models. Acute treatment with the OM-3 fatty acid docosahexaenoic acid suppressed MSU-, cholesterol crystal-, and calcium pyrophosphate crystal-mediated interleukin-1β (IL-1β) production in vitro. In vivo, OM-3 CA dose-dependently reduced crystal-mediated cell migration, exudate volume, and levels of IL-1β and prostaglandin E2. Following intra-articular injection of MSU, treatment with OM-3-CA (1 mL/kg) and indomethacin (1 mg/kg) resulted in similar mean reductions in pain (23% and 41%, respectively) and swelling (58% and 50%, respectively), compared with controls. Additionally, in complex formulations of OM-3 fatty acids, high levels of palmitic acid could reduce the in vivo effect on crystal-mediated IL-1β elevation. OM-3 CA has a broadly efficacious anti-inflammatory effect with a strong exposure–response relationship that could be beneficial in prevention and treatment of crystal arthritis, with potential applications in other IL-1β-mediated diseases.

Serotonin Exhibits Accelerated Bleomycin-Induced Pulmonary Fibrosis through TPH1 Knockout Mouse Experiments.

Background Pulmonary fibrosis is a chronic progressive fibrosis interstitial lung disease that is characterized by inflammatory infiltration and fibrotic changes. 5-Hydroxytryptamine (5-HT) is an important regulatory factor in inflammation, immunomodulation, and fibrosis. The aim of this study was to investigate the role of 5-HT in bleomycin- (BLM-) induced pulmonary fibrosis through wild-type C57BL/6 (WT) and TPH1 knockout (KO) mouse experiments. Methods The mice were grouped as follows: WT control group, KO control group, WT BLM group, and KO BLM group. Mice were administrated bleomycin hydrochloride through intratracheal instillation to induce pulmonary fibrosis. Mice were sacrificed 0, 7, 14, and 21 days after modeling, and bronchoalveolar lavage fluid (BALF) and lung tissues were collected to determine the severity of fibrotic changes. Results The results showed that the weight loss of mice in the WT BLM group was more severe than that in the KO BLM group. H&E and Sirius Red staining revealed that 5-HT markedly aggravated histological damage and fibrotic changes in the lung. Significantly lower levels of hydroxyproline, Ashcroft fibrosis score, total BALF protein and cells, BALF tumor necrosis factor- (TNF-) α and interleukin- (IL-) 6, TNF-α and IL-6 mRNA, malondialdehyde (MDA), and myeloperoxidase- (MPO-) positive cells in the lung tissues, and fibrosis-associated proteins were discovered in the mice from the KO BLM group compared with the WT BLM group. Conclusion 5-HT aggravated pulmonary fibrosis mainly by promoting the inflammation, exudation of proteins and cells, oxidative stress, and upregulation of fibrosis-associated genes in the lung tissues.

Isoliquiritigenin Activates Nuclear Factor Erythroid-2 Related Factor 2 to Suppress the NOD-Like Receptor Protein 3 Inflammasome and Inhibits the NF-κB Pathway in Macrophages and in Acute Lung Injury

Among the cellular response mechanisms, the nuclear factor erythroid-2 related factor 2 (Nrf2) pathway is considered a survival pathway that alleviates oxidative injury, while both the NOD-like receptor protein 3 (NLRP3) and NF-κB pathways are pro-inflammatory pathways that cause damage to cells. These pathways are implicated in the development and resolution of acute lung injury (ALI). Isoliquiritigenin (ISL), a flavonoid from the liquorice compound, is suggested to be a regulator of the above pathways, but the mechanisms of how the NLRP3/NF-κB pathway interacts with Nrf2 and its protective effects in ALI remain unknown. In the present study, ISL inhibited reactive oxygen species (ROS) generation and cytotoxicity induced by t-BHP and pro-inflammatory enzymes production induced by LPS in RAW 264.7 cells. Such cytoprotective effects coincided with the induction of AMP-activated protein kinase (AMPK)/Nrf2/antioxidant response element (ARE) signaling and the suppression of the NLRP3 and NF-κB pathways. Consistent with these findings, ISL treatment significantly alleviated lung injury in LPS-induced ALI mice, which was reflected by reductions in histopathological changes, pulmonary edema, and protein leakage. At the same time, the increased levels of inflammatory cell exudation and pro-inflammatory mediators, the enhanced production of ROS, myeloperoxidase, and malondialdehyde, and the depleted expression of GSH and superoxide dismutase induced by LPS were ameliorated by ISL. Furthermore, ISL notably activated AMPK/Nrf2/ARE signaling and inhibited LPS-induced NLRP3 and NF-κB activation in the lung. Moreover, although inhibition of the LPS-induced histopathological changes and ROS production were attenuated in Nrf2-deficient mice, the repression of the NLRP3 and NF-κB pathways by ISL was Nrf2-dependent and Nrf2-independent, respectively. In conclusion, our results are the first to highlight the beneficial role and relevant mechanisms of ISL in LPS-induced ALI and provide novel insight into its application.

Marine Microbial Polysaccharides Environmental role and Applications: An Overview

Marine habitat represents about 70% of our planet. Microbial populations including bacteria, fungi and algae represent a base of food pyramids in this environment. The exudates of microbial cells (like polysaccharide) in the marine environment play an important role in energy cycling between the surface and the bottom in the sea by aggregation of small molecules causing them to sink. So it plays an important role in carbon sequestration and re emission through what called biologic pump. On the other hand, microbial polysaccharides help the microbial cell itself to colonize hydrophobic surfaces forming biofilms and tolerate drastic conditions like heat, salinity and cold stresses. Marine microbial polysaccharides are characterized by unique properties making them a good source of bioactive agents that can be used in many fields as anti-tumor, antiviral, antioxidant, anticoagulant, food and feed applications. An overview of the role of polysaccharide in the marine environment, its advantages and applications will be presented.

Determination of phenolic profile by HPLC-ESI-MS/MS and anti-inflammatory activity of crude hydroalcoholic extract and ethyl acetate fraction from leaves of Eugenia brasiliensis

Eugenia brasiliensis Lam., Myrtaceae, is used in folk medicine for anti-inflammatory diseases such as arthritis and rheumatism. This study investigated the anti-inflammatory activity and phenolic profile of the crude hydroalcoholic extract and ethyl acetate fraction from E. brasiliensis leaves. Crude hydroalcoholic extract and the ethyl acetate fraction were analyzed by HPLC-ESI-MS/MS in comparison to standard phenolic compounds. The anti-inflammatory activity of the crude hydroalcoholic extract (1, 10 and 25mgkg−1) and the ethyl acetate fraction (10, 25 and 50mgkg−1) was evaluated in a swiss mouse model of acute pleurisy induced by carrageenan, being the total cell count, exudation and analysis of nitrite/nitrate the inflammation parameters. HPLC-ESI-MS/MS analysis revealed apigenin, catechin, galangin, isoquercetin, myricetin, quercetin and rutin. Crude hydroalcoholic extract and ethyl acetate fraction were effective in inhibiting cell migration in all tested doses. Crude hydroalcoholic extract was effective in inhibiting exudation only at the 10mgkg−1 dose; ethyl acetate fraction was effective in all tested doses. Results for nitrite/nitrate levels reveals that only the ethyl acetate fraction was effective at the tested doses. This is the first report of the presence of isoquercetin, galangin and apigenin in this species. Results from the phytochemical analysis enhance the chemical knowledge of this species. In the future, together with more studies, validation of its popular use in inflammatory diseases is possible.

Effects of Trichilia monadelpha (Meliaceae) extracts on bone histomorphology in complete Freund's adjuvant-induced arthritis

This study aimed to assess the effect of petroleum ether extract (PEE), ethyl acetate extract (EthE), and ethanol extract (EAE) of Trichilia monadelpha stem bark on bone histomorphology in arthritis. Percentage inhibition of edema and arthritic scores in complete Freund's adjuvant-induced (0.1 ml of 5 mg/ml1 of heat-killed Mycobacterium tuberculosis in paraffin oil-injected subplantar into the right hind paw) arthritic Sprague-Dawley rats treated with PEE, EthE, or EAE (10,30, and 100 mg/kg1, respectively), dexamethasone (0.3-3.0 mg/kg1), or methotrexate (0.1-1.0 mg/kg1) over a 28-day period were estimated. Rat paws were radiographed and scored. Body weights were taken and paw tissues were harvested for histopathological studies. The extracts significantly (P ≤ 0.01-0.0001) and dose dependently reduced the polyarthritic phase of arthritis. EAE and PEE significantly (P ≤ 0.01-0.0001) minimized edema spread from acute arthritic phase (days 0-10) to polyarthritic phase (days 10-28). EthE improved which deteriorated body weight in arthritis. All extracts significantly (P ≤ 0.05-0.01) improved arthritic score; reducing erythema, swelling and joint rigidity, and also significantly (P ≤ 0.05-0.01) reduced hyperplasia, pannus formation, and exudation of inflammatory cells into synovial spaces. The stem bark extracts of T. monadelpha reduce bone tissue damage and resorption associated with adjuvant-induced arthritis, hence could be useful in managing arthritis in humans.

Phytochemical study and anti-inflammatory effect of Psychotria stenocalyx (Rubiaceae)

Anti-inflammatory activity of fractionated extracts of Salvia officinalisValeria Dal Pra, Lais B. Bisol, Suelen Detoni, Marjorie Denti, Jaine Grando, Camila Pollo, Tiago R. Pasquali, Arno Ernesto Hoffmann, Marcio A. Mazutti, Sandra M. D. Macedo

Primary idiopathic osteoarthropathy.

A 49-year-old man presented with arthralgias and effusion of the knees. His past medical syndrome revealed digital clubbing for 17 years (A) and an idiopathic Raynaud syndrome. Radiographs of the tibias and fibulas showed bilateral, symmetric, extended and multilayered periosteal thickening (B). Thoracic CT and cardiac ultrasound were normal, as well as inflammatory, hepatic and renal tests. Infectious investigations were negative. The diagnosis of primary idiopathic osteoarthropathy (HOA) was made with 3-year follow-up. HOA is a syndrome characterized by three clinical features: digital clubbing (also termed Hippocratic fingers), periostosis of tubular bones, and synovial effusions. HOA can be a primary entity, or can be secondary to extra skeletal conditions. Primary HOA is a rare disease, with male predilection. Hippocratic fingers show a distinctive bulbous deformity of the fingertips. It can be associated with large joint’s effusions but there is neither synovial membrane hypertrophy nor inflammatory cell exudation. Radiographs may show an acro-osteolysis, periostosis of tubular bones. The tibia, fibula, radius, and ulna are the most commonly affected bones.

Antioxidant activity of Cornelian cherry (Cornus mas L.) fruits extract and the in vivo evaluation of its anti-inflammatory effects

The biological activity of Cornus mas fruits (CM) on acute inflammation in relation to the in vitro antioxidant properties was investigated. The in vitro antioxidant activity was evaluated by ferric reducing ability of plasma (FRAP) and by the 2,2′-azinobis-3-ethyl-benzthiazino-6-sulphonic acid (ABTS) test. The high-performance liquid chromatography (HPLC) profile of CM extract revealed the presence of 10 main phenolic compounds. The anti-inflammatory effect of CM extract was evaluated by analysing the cytokine levels in the soft paw tissue of Wistar rats after inducing inflammation. CM extract showed potent in vitro antioxidant activity and also led to significant suppression of interleukin (IL)-1β and IL-13 production in paw tissue, enhancing the production of IL-10. The histopathological investigation of paw and liver samples revealed that low dose of CM extract attenuated the initial acute inflammatory reaction while high dose inhibited the exudation of inflammatory cells to the inflammation site.

Inhibition of the NF-κB and p38 MAPK pathways by scopoletin reduce the inflammation caused by carrageenan in the mouse model of pleurisy

Natural products have long been used worldwide as therapeutic agents, but it is only recently, in response to the new challenges posed by global population aging, that interest in research into potentially therapeutic natural products has reemerged. In this context, coumarins, chemical compounds found in plants that have known anti-inflammatory activity, are promising candidates for the development of new drugs. In this study we test the effect of scopoletin, a coumarin found in several plant species, on carrageenan-induced inflammation in the mouse model of pleurisy. Initially, the effects of scopoletin on leukocyte migration and exudate concentrations were evaluated at three different doses (0.1, 1 and 5 mg/kg) and time (0.5–4 h before pleurisy). In the next step, we chose the lowest dose capable of inhibiting the inflammatory parameters (1 mg/kg), in order to analyze the myeloperoxidase and adenosine deaminase activities, the nitric oxide, tumor necrosis factor-α, and interleukin 1β levels in the fluid leakage, and the p65 subunit of NF-κB and p38 MAPK phosphorylation. Scopoletin at a dose of 1 mg/kg was able to significantly reduce cell migration and exudation to the pleural fluid (p < 0.01). Scopoletin at the same dose also decreased the myeloperoxidase and adenosine-deaminase activities and nitric oxide, tumor necrosis factor-α, and interleukin-1β levels (p < 0.01). In addition, it significantly reduced p65 and p38 phosphorylation in the mouse lungs (p < 0.01). Our results reinforce that scopoletin has important anti-inflammatory activity, and shows, that this effect can be attributed to the ability of this compound to inhibit the phosphorylation of NF-κB and p38 MAPK.