Cecropia hololeuca: A new source of compounds with potential anti-inflammatory action.

Our objective is to investigate the phytochemical components, antioxidant capacity and in vitro and in vivo anti-inflammatory action from Cecropia hololeuca bark aqueous extract (AECh). The chemical characterization of AECh was performed through CE-UV, FTIR and NMR Spectroscopy. In vitro assays were performed with the AECh on murine macrophages J774A.1 cells in order to analyse cell viability, NO, TNF-α and IL-1ß productions and the in vivo anti-inflammatory potential in acute carrageenan paw oedema in mice. The AECh showed a decrease in the production of NO, TNF-α and IL-1ß, without altering the cell viability and reduction of the paw thickness in the 2nd, 3rd and 4th hour. The extract presented 72% free radical scavenging, 0.60% flavonoid content and showed the presence of gallic acid, caffeic acid and catechin as major constituents. The C. hololeuca bark extract showed important antioxidant and anti-inflammatory activity, emphasizing the industrial and pharmacological potential of this plant.

Genistein modulates the expression of Toll-like receptors in experimental autoimmune encephalomyelitis.

OBJECTIVE AND DESIGN: The present work investigates the modulation of experimental autoimmune encephalomyelitis (EAE) using genistein before the EAE induction. MATERIAL: Female C57BL/6 mice (n = 96 mice/experiment), 4-6 weeks old, were used to induce the EAE. The mice were divided into three experimental groups: non-immunized group, immunized group (EAE), and immunized and treated with genistein group (Genistein). TREATMENT: Genistein was used at a dose of 200 mg/kg s.c. and were initiated 2 days before the immunization and continued daily until day 6 postimmunization. METHODS: Animals were monitored daily for clinical signs of EAE up to day 21. Inflammatory infiltration, demyelination, Toll-like receptor (TLR) expression, cytokines and transcription factors were analyzed in spinal cords. RESULTS: The present study demonstrates, for the first time, the genistein ability to modulate the factors involved in the innate immune response in the early stages of EAE. The genistein therapy delayed the onset of the disease, with reduced inflammatory infiltration and demyelination. In addition, the expression of TLR3, TLR9 and IFN-ß were increased in genistein group, with reduction in the factors of TH1 and Th17 cells. CONCLUSION: These findings shed light on the potential of genistein as a prophylactic strategy for multiple sclerosis (MS) prevention.

Ferulic acid supresses Th2 immune response and prevents remodeling in ovalbumin-induced pulmonary allergy associated with inhibition of epithelial-derived cytokines.

Asthma is characterized by intermittent airway obstruction and chronic inflammation, orchestrated primarily by Th2 cytokines. There is a strong rationale for developing new asthma therapies, since current treatment protocols present side effects and may not be effective in cases of difficult-to-control asthma. The purpose of this study was to evaluate the effect of ferulic acid, a phenolic acid commonly present in plants, in the ovalbumin-induced pulmonary allergy murine model. METHODS: BALB/c mice were sensitized and challenged with ovalbumin, and treatments were provided by gavage. Six groups of mice (n = 6) were studied, labeled as: control, pulmonary allergy, dexamethasone, and 3 receiving ferulic acid (at 25, 50, and 100 mg/kg). Lung tissue, bronchoalveolar lavage fluid and serum were collected for analysis. RESULTS: Ferulic acid treatment inhibited an established allergic Th2-response by decreasing the key features of pulmonary allergy, including lung and airway inflammation, eosinophil infiltration, mucus production and serum levels of OVA-specific IgE. These results were associated with lower levels of CCL20, CCL11 and CCL5 chemokines and IL-4, IL-5, IL-13, TSLP, IL-25 and IL-33 cytokines in lung tissue homogenate. CONCLUSIONS: In this study it was demonstrated for the first time that ferulic acid treatment is able to suppress one of the main features of the airway remodeling, indicated by reduction of mucus production, besides the Th2 pathogenic response on ovalbumin-induced pulmonary allergy. Taken together, results shows that the immunopathological mechanism underlying these effects is linked to a reduction of the epithelial-derived chemokines and cytokines, suggesting that ferulic acid may be useful as a potential therapeutic agent for asthma.

Inhibiting AKT phosphorylation employing non-cytotoxic anthraquinones ameliorates TH2 mediated allergic airways disease and rhinovirus exacerbation.

BACKGROUND: Severe asthma is associated with T helper (TH) 2 and 17 cell activation, airway neutrophilia and phosphoinositide-3-kinase (PI3K) activation. Asthma exacerbations are commonly caused by rhinovirus (RV) and also associated with PI3K-driven inflammation. Anthraquinone derivatives have been shown to reduce PI3K-mediated AKT phosphorylation in-vitro. OBJECTIVE: To determine the anti-inflammatory potential of anthraquinones in-vivo. METHODS: BALB/c mice were sensitized and challenged with crude house dust mite extract to induce allergic airways disease and treated with mitoxantrone and a novel non-cytotoxic anthraquinone derivative. Allergic mice were also infected with RV1B to induce an exacerbation. RESULTS: Anthraquinone treatment reduced AKT phosphorylation, hypoxia-inducible factor-1α and vascular endothelial growth factor expression, and ameliorated allergen- and RV-induced airways hyprereactivity, neutrophilic and eosinophilic inflammation, cytokine/chemokine expression, mucus hypersecretion, and expression of TH2 proteins in the airways. Anthraquinones also boosted type 1 interferon responses and limited RV replication in the lung. CONCLUSION: Non-cytotoxic anthraquinone derivatives may be of therapeutic benefit for the treatment of severe and RV-induced asthma by blocking pro-inflammatory pathways regulated by PI3K/AKT.

Influence of salivary secretory immunoglobulin A level on the pain experienced by orthodontic patients.

BACKGROUND: Pain, a common experience reported by patients under orthodontic treatment, results from force application to the teeth and trauma caused by attrition of brackets and wires against the underlying oral mucosa. The main protection of the mucosa is secretory immunoglobulin A (sIgA), which may play a fundamental role in integrity maintenance and whose production may be reduced as a result of the stress of orthodontic treatment. The aim of this study was to assess sIgA levels in the saliva and their correlation with oral pain intensity in adults and children after the installation of fixed orthodontic appliances. MATERIAL/METHODS: Twenty patients (10 children, age 11-13 years; 10 adults, age 18-37 years) were assessed before treatment, after bracket bonding, and after initial arch wire insertion. Saliva was sampled for sIgA analysis, and oral pain was assessed through a visual analog scale. RESULTS: Although there was a trend toward reduction of the salivary sIgA levels during the initial arch phase in the children, and during the bonding and initial arch phases in the adults, this finding was not significant. CONCLUSIONS: There was a trend toward a negative correlation of oral pain intensity and salivary sIgA levels in the children, which may indicate the importance of sIgA for oral protection during orthodontic treatment, interfering with the pain experienced by the patients.