Prevalence of metabolic syndrome and its association with risk factors in patients with established atherosclerosis disease.

Risk factors can lead to clinical conditions, like metabolic syndrome, that predisposes the development of cardiovascular diseases. The aim of this study was to describe the prevalence and which risk factors cause more impact in metabolic syndrome in patients with established atherosclerosis disease. A cross-sectional study was performed as a subanalysis of Programa Alimentação Cardioprotetora Brasileira. Weight, height, waist circumference, blood pressure, lipid profile and fasting glucose were collected. Metabolic syndrome was defined according to the harmonized criteria. Linear regression was used to analyze the association between number of components of metabolic syndrome and risk factors. 82 patients were included and the prevalence of metabolic syndrome was 84.1%. Being overweight was associated with an increase by 0.55 point in diagnostic criteria of metabolic syndrome in crude analysis (95%CI 0.09-1.00) and 0.64 in adjusted analysis (95%CI 0.18-1.09), while former/current smoker status was responsible for raising by 0.48 the number of components of metabolic syndrome, only in adjusted analysis (95%CI 0.04-0.92). Overweight and former/current smoker status are associated with MS, increasing the probability of atherosclerotic events. A healthy lifestyle, that includes avoiding tobacco exposure and proper weight control, must be encouraged in this high-risk population.

Genoprotective effects of the green tea-derived polyphenol/epicatechin gallate in C6 astroglial cells.

In vitro and in vivo studies have recently reported significant chemopreventive effects of green tea-derived polyphenols in different diseases. However, it remains unclear how such effects could be triggered. In order to elucidate the effects of epicatechin gallate (ECG) in C6 cells, both by itself and against H2O2-induced genotoxicity, measurements of DNA strand breaks and chromosome loss were performed. DNA damage was measured by comet and micronucleus assays. The present study shows for the first time how ECG, the major green tea-derived polyphenol, is able to exert dose-dependent genoprotective effects in an H2O2-induced toxicity model of C6 astroglial cells. We demonstrate that doses of ECG in a range from 0.1 to 1 µM were able to completely prevent H2O2-induced genotoxicity in vitro. In contrast, considerably higher concentrations of ECG (10 µM) were able to reverse previous positive effects in a dose- and time-dependent manner. The same results were confirmed by both comet (F(3,9) = 336,148; P < .001) and micronucleus (F(3,9) = 23,228; P < .001) methods. Together, our data show ECG as a dose-dependent genoprotective compound in C6 astroglial cells. This indicates that small doses of polyphenols included in our diet could have beneficial effects on neural cells, contributing to prevention of oxidative stress-associated brain pathologies. In addition, our data highlight the importance of strictly modulating doses and/or consumption of antioxidant-fortified foods or additional supplements containing such beneficial molecules.

Epicatechin gallate increases glutamate uptake and S100B secretion in C6 cell lineage.

There is a current interest in dietary compounds, such as green tea polyphenols, that can favor protection against a variety of brain disorders, including Alzheimer's disease, ischemia, and stroke. The objective of the present study was to investigate the effects of (-)-epicatechin-3-gallate (ECG), one of three three major green tea antioxidants, on C6 lineage cells. Here, we evaluated cell morphology and integrity and specific astrocyte activities; glutamate uptake and secretion of S100B in the presence of 0.1, 1 and 10 microM ECG. During 6 h of incubation, cell morphology was altered only at 10 microM ECG; however, after 24 h of treatment, cells become stellate in the presence of all concentrations of ECG. Loss of cell integrity was observed after 24 h with 10 microM ECG and represented only 6% of cells, in contrast with 2% observed at basal conditions. ECG (1-10 microM) induced a decrease (about 36%) in glutamate uptake after 1 h of incubation. After 6 h, an opposite effect occurred and ECG induced a sustained increase in glutamate uptake of about 70% from 0.1 microM. In addition, a significant increase in S100B was observed at 1 microM ECG (36%) and 10 microM ECG (69%) after 1 h, in contrast to 6 h of treatment, where all doses of ECG induced a significant increase (about 60%) in S100B secretion. These data demonstrate that ECG induces a significant improvement in glutamate uptake and S100B secretion in C6 cells, indicating that ECG could contribute to the neuroprotective role of astroglial cells.