RESUMO
The appearance of resistant bacteria was found to reduce the efficiency of antimicrobial therapies with the current antibiotics, thereby increasing the need for more efficient drugs for the treatment of infections. Several studies have demonstrated an increase in antimicrobial activity following the interaction of several compounds with metal ions. The present study used a methodology adapted for antimicrobial bioassays using plant extracts, in compliance with the standards of the Clinical and Laboratory Standards Institute against Gram-positive and Gram-negative bacteria. The results obtained were considered appropriate for determining MIC, MBC as for performing antimicrobial sensitivity testing with good efficiency and reproducibility. The bacteria Pseudomonas fluorescens exhibited high sensitivity to the tested compounds, being efficient to evaluate the antibacterial activity. The bioassays with the metal complexes of flavonoid quercetin and Ga(III) ions, and synthetic ligand H2bbppd and Cu(II) ions showed a greater inhibitory effect than their individual ligands, thus, the addition indicated an increase in the antimicrobial activity after the coordination. Both metal complexes exhibit good antimicrobial performances, such as low minimum inhibitory concentration (MIC ≤ 250 µg/ml), bactericidal effect and a broad activity spectrum, which qualify these compounds as suitable candidates to the next step of drugs fabrication. Nevertheless, further studies on the mechanism of growth inhibition and toxicity are needed, in order to evaluate the potential of therapeutic application.
RESUMO
Current techniques to resolve heart valve defects involve the use of prosthetic and bioprosthetic materials. These materials lack the potential to grow and are not ideal, especially not for pediatric patients. Novel techniques like tissue engineering involve the use of biodegradable polymers coated with autologous myofibroblast and endothelial cells. We inspected morphological and marker gene expression differences between cells harvested from the saphenous vein, or from veins and arteries of the umbilical cord, and the cells they are designed to replace: the interstitial and endothelial cells of the pulmonary heart valve. We assessed the extent to which the endothelial cells from the inspected sources in vitro resemble endothelial cells of human pulmonary heart valves, and we found that myofibroblast cells, respective of their source, in vitro differ from the interstitial cells from human pulmonary heart valves regarding collagen and smooth muscle alpha-actin. Therefore we conclude that the cells isolated from the saphenous veins, or from veins and arteries of the umbilical cord might be feasible cell sources for tissue engineering of heart valve for the pulmonary position.
Assuntos
Células Endoteliais/citologia , Valvas Cardíacas/citologia , Valva Pulmonar/citologia , Engenharia Tecidual/métodos , Biomarcadores/análise , Expressão Gênica , Doenças das Valvas Cardíacas/terapia , Humanos , Imuno-Histoquímica , Imunofenotipagem , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Veia Safena/citologia , Veias Umbilicais/citologiaRESUMO
Diabetes is associated with an enhanced collagen-mediated platelet activation that contributes significantly to thromboischemic complications. In this study, the platelet collagen receptor glycoprotein VI (GPVI) was studied in 385 patients with type 2 diabetes. Surface expression of the platelet Fc receptor that forms a functional complex with GPVI was significantly increased in patients with diabetes compared with those without diabetes (P = 0.02). Fc receptor expression correlated with GPVI expression and was found to be independently associated with diabetes (r = 0.529, P < 0.001). Stimulation of GPVI through a specific anti-GPVI monoclonal antibody significantly enhanced surface expression of CD40L (P = 0.006). Because CD40L is a potent platelet-derived cytokine that is involved in thrombosis and atherosclerosis, we evaluated the effect of GPVI-mediated release of CD40L on activation of endothelial cells. Coincubation of GPVI-stimulated platelets resulted in substantial enhanced endothelial surface expression of CD62P, alphavbeta3, and intercellular adhesion molecule 1 (P < 0.05) and secretion of monocyte chemoattractant protein 1 of cultured human umbilical vein endothelial cells (P < 0.01). These results suggest that the function of collagen receptor GPVI is altered in type 2 diabetes and may play an important role in atherothrombotic complications. Inhibition of GPVI may be a promising pharmacological target in the treatment of high-risk diabetic patients.