Absence of mutagenicity and antimutagenicity of the extract obtained from the flowers of "ipê roxo" Tabebuia impetiginosa (Mart. ex DC.) Standl

A Tabebuia impetiginosa, conhecida popularmente como ipê-roxo, é uma planta nativa das florestas tropicais chuvosas da América do Sul e Central. Componentes químicos obtidos da casca têm mostrado efeito terapêutico, como antiinflamatório, antifúngico e antibacteriano. Porém, pela falta de dados na literatura, pouco se sabe sobre os efeitos do extrato das flores. Assim, o objetivo do presente trabalho foi avaliar o potencial mutagênico e antimutagênico do extrato obtido das flores da T. impetiginosa, em três diferentes concentrações (100, 300 e 500 mg kg-1 p.c.) pelo teste do micronúcleo. Para o teste de mutagenicidade, a doxorrubicina (DXR, 90 mg kg-1 p.c.) foi utilizada como indutor de danos no DNA e para o teste de antimutagenicidade, os tratamentos com o extrato foram realizados simultaneamente com este agente químico. O sangue periférico dos animais foi coletado 24 horas após os tratamentos. A comparação da frequência de eritrócitos policromáticos (PCEs) em 400 eritrócitos/animal entre os diferentes grupos não demonstrou qualquer citotoxicidade do extrato. Em relação às frequências de micronúcleos em PCEs (PCEMNs), não foram observadas diferenças significativas entre os grupos tratados com as diferentes concentrações de extrato e o controle negativo. Da mesma forma, todos os grupos de animais que receberam os tratamentos simultâneo do extrato (100, 300 ou 500 mg kg-1 p.c.) com a DXR, apresentaram valores de PCEMNs muito próximos quando comparados com os dados observados no grupo de animais que recebeu somente a DXR. Esses resultados apresentados indicam ausência de efeito mutagênico e antimutagênico do extrato obtido das flores da T. impetiginosa em sistema teste in vivo.T. impetiginosa, known as "ipê-roxo", is a plant native to tropical rain forests of Central and South Americas. Chemical compounds obtained from its bark have shown anti-inflammatory, antifungal and antibacterial therapeutic effect. However, due to the lack of data in the literature, little is known about the effects of its flower extract. Thus, the aim of this study was to evaluate the mutagenic and antimutagenic potential of the extract obtained from T. impetiginosa flowers at three different concentrations (100, 300 and 500 mg kg-1 p.c.) by the micronucleus test. For the mutagenicity test, doxorubicin (DXR, 90 mg kg-1 p.c.) was used as DNA-damage inducer, while for the antimutagenicity test, treatments with the extract were performed simultaneously with this chemical agent. The peripheral blood of animals was collected 24 hours after the treatments. The frequency of polychromatic erythrocytes (PCEs) in 400 erythrocytes/animal was compared among the different groups and showed no extract cytotoxicity. As regards the frequency of micronuclei in PCEs (PCEMNs), there were no significant differences between the groups treated with different concentrations of extract and the negative control. Similarly, all groups of animals that received the simultaneous extract treatments (100, 300 or 500 mg kg-1 p.c.) with DXR showed very similar values of PCEMNs when compared with the data observed for the group of animals that received DXR alone. These results indicate no mutagenic and antimutagenic effect of the extract obtained from T. impetiginosa flowers in the testing system in vivo.Conselho Nacional de Desenvolvimento Cientifico e Tecnológico (CNPq

The inflammatory stimulus of a natural latex biomembrane improves healing in mice

The aim of the present study was to compare healing obtained with biomembranes with the natural healing process (sham) using biochemical and immunohistological assays. C57BL/6 mice were divided into 4 groups of 15 mice each and received different subcutaneous implants: natural latex biomembrane (NLB), denatured latex (DL), expanded polytetrafluorethylene (ePTFE), or sham. On the 2nd, 7th, and 14th days post-treatment, 5 mice per group were sacrificed and biopsied for the following measurements: oxidative stress based on malondialdehyde (MDA), myeloperoxidase (MPO) and hydrogen peroxide by the method of ferrous oxidation-xylenol orange (FOX), as well as glutathione and total proteins; histological evaluation to enumerate inflammatory cells, fibroblasts, blood vessels, and collagen, and immunohistochemical staining for inducible nitric oxide synthase, interleukin-1&#946;, vascular endothelial growth factor (VEGF), and transforming growth factor-&#946;1 (TGF-&#946;1). On day 2 post-treatment, NLB stimulated a dense inflammatory infiltrate mainly consisting of polymorphonuclear cells, as indicated by increased MPO (P < 0.05), but oxidative stress due to MDA was not observed until the 7th day (P < 0.05). The number of blood vessels was greater in NLB (P < 0.05) and DL (P < 0.05) mice compared to sham animals on day 14. NLB induced fibroplasia by day 14 (P < 0.05) with low expression of TGF-&#946;1 and collagenesis. Thus, NLB significantly induced the inflammatory phase of healing mediated by oxidative stress, which appeared to influence the subsequent phases such as angiogenesis (with low expression of VEGF) and fibroplasia (independent of TGF-&#946;1) without influencing collagenesis

Efficacy of the dietary histone deacetylase inhibitor butyrate alone or in combination with vitamin A against proliferation of MCF-7 human breast cancer cells

The combined treatment with histone deacetylase inhibitors (HDACi) and retinoids has been suggested as a potential epigenetic strategy for the control of cancer. In the present study, we investigated the effects of treatment with butyrate, a dietary HDACi, combined with vitamin A on MCF-7 human breast cancer cells. Cell proliferation was evaluated by the crystal violet staining method. MCF-7 cells were plated at 5 x 10(4) cells/mL and treated with butyrate (1 mM) alone or combined with vitamin A (10 µM) for 24 to 120 h. Cell proliferation inhibition was 34, 10 and 46% following treatment with butyrate, vitamin A and their combination, respectively, suggesting that vitamin A potentiated the inhibitory activities of butyrate. Furthermore, exposure to this short-chain fatty acid increased the level of histone H3K9 acetylation by 9.5-fold (Western blot), but not of H4K16, and increased the expression levels of p21WAF1 by 2.7-fold (Western blot) and of RAR&#946; by 2.0-fold (quantitative real-time PCR). Our data show that RAR&#946; may represent a molecular target for butyrate in breast cancer cells. Due to its effectiveness as a dietary HDACi, butyrate should be considered for use in combinatorial strategies with more active retinoids, especially in breast cancers in which RAR&#946; is epigenetically altered

Assessment of indicators of vitamin A status in non-cirrhotic chronic hepatitis C patients

Subjects with chronic liver disease are susceptible to hypovitaminosis A due to several factors. Therefore, identifying patients with vitamin deficiency and a requirement for vitamin supplementation is important. Most studies assessing vitamin A in the context of hepatic disorders are conducted using cirrhotic patients. A cross-sectional study was conducted in 43 non-cirrhotic patients with chronic hepatitis C to evaluate markers of vitamin A status represented by serum retinol, liver retinol, and serum retinol-binding protein levels. We also performed the relative dose-response test, which provides an indirect estimate of hepatic vitamin A reserves. These vitamin A indicators were assessed according to the stage of liver fibrosis using the METAVIR score and the body mass index. The sample study was predominantly composed of male subjects (63%) with mild liver fibrosis (F1). The relative dose-response test was <20% in all subjects, indicating vitamin A sufficiency. Overweight or obese patients had higher serum retinol levels than those with a normal body mass index (2.6 and 1.9 µmol/L, respectively; P<0.01). Subjects with moderate liver fibrosis (F2) showed lower levels of serum retinol (1.9 vs 2.5 µmol/L, P=0.01) and retinol-binding protein levels compared with those with mild fibrosis (F1) (46.3 vs 67.7 µg/mL, P<0.01). These results suggested an effect of being overweight on serum retinol levels. Furthermore, more advanced stages of liver fibrosis were related to a decrease in serum vitamin A levels