Mindfulness-based intervention for college faculties and students in Brazil.

Background: Teacher and students' stress has been a challenge in education. An approach to stress reduction is mindfulness training. The Mindfulness-based stress reduction (MBSR) has been used to improve the condition of individuals with various health outcomes. The aim of this study was to examine whether MBSR may improve depression, well-being, and perceived stress of Brazilian college faculty and students. Methods: MBSR was performed with college faculty and students from Centro Universitario de Belo Horizonte (UniBH). Participants answered questionnaires (Psychological General Well-Being Index, Perceived Stress Scale, and Beck Depression Index) at the beginning and end of the intervention. A control group of teachers also answered the questionnaires but did not participate in the MBSR intervention. Statistical analyses were performed using paired Student's t-test (P < 0.05 significance). Results: The MBSR intervention positively impacted all conditions measured in the questionnaires in faculty and students who attended the intervention. Faculty and students in the control group had shown conditions being maintained or worsened. Discussion: The MBSR was effective as faculty and students from the experimental group exhibited improvement in general well-being, depression levels, and perceived stress after attending the intervention.

Ascorbic acid, alpha-tocopherol, and beta-carotene reduce oxidative stress and proinflammatory cytokines in mononuclear cells of Alzheimer's disease patients.

OBJECTIVES: The in vitro effect of a vitamin complex in generating and reducing oxidative species in peripheral blood mononuclear cells (PBMNC) and plasma of patients with Alzheimer's disease (AD) and healthy subjects (HS) was evaluated. METHODS: Two concentrations of a vitamin complex ([A] and [20A]) with ascorbic acid, alpha-tocopherol, and beta-carotene were incubated with either mononuclear cells or plasma. The generation of oxidizing species was measured in a luminol-dependent chemiluminescence assay and the reducing response by the MTT dye reduction assay. The levels of cytokines (interleukin [IL]-1ß, IL-6, and IL-4) were measured by sandwich enzyme-linked immunosorbent assay. RESULTS: Our results demonstrated that the increase in the vitamin complex concentration reduced the reactive oxygen species (ROS) production and enhanced cellular reduction capacity in cells of AD patients in concentration [20A]. Plasma reduction capacity rose significantly for both groups (AD and HS). Concentration [A] did not alter the IL-1ß production, increased IL-4 production in both groups and lowered IL-6 production in AD cells. Concentration [20A] increased pro-inflammatory cytokines (IL-1ß and IL-6) and decreased IL-4 production by PBMNC of HS leading to a pro-inflammatory status. DISCUSSION: The antioxidant vitamin complex was effective in reducing oxidative stress in PBMNC of AD patients by lowering ROS production, improving cellular antioxidant capacities and modifying cytokine induced inflammation.

The production of nitric oxide, IL-6, and TNF-alpha in palmitate-stimulated PBMNCs is enhanced through hyperglycemia in diabetes.

We examined nitric oxide (NO), IL-6, and TNF-α secretion from cultured palmitate-stimulated PBMNCs or in the plasma from type 2 diabetes mellitus (T2MD) patients or nondiabetic (ND) controls. Free fatty acids (FFA) have been suggested to induce chronic low-grade inflammation, activate the innate immune system, and cause deleterious effects on vascular cells and other tissues through inflammatory processes. The levels of NO, IL-6, TNF-α, and MDA were higher in supernatant of palmitate stimulated blood cells (PBMNC) or from plasma from patients. The results obtained in the present study demonstrated that hyperglycemia in diabetes exacerbates in vitro inflammatory responses in PBMNCs stimulated with high levels of SFA (palmitate). These results suggest that hyperglycemia primes PBMNCs for NO, IL-6, and TNF-alpha secretion under in vitro FFA stimulation are associated with the secretion of inflammatory biomarkers in diabetes. A combined therapy targeting signaling pathways activated by hyperglycemia in conjunction with simultaneous control of hyperglycemia and hypertriglyceridemia would be suggested for controlling the progress of diabetic complications.

Suppressive effect of aqueous humor from person with type 2 diabetes with or without retinopathy on reactive oxygen species generation.

AIM: To evaluate the antioxidant capacity and concentrations of vascular endothelial growth factor (VEGF) and interleukin 6 (IL-6) in aqueous humor from patients with type 2 diabetes mellitus (T2DM) with or without retinopathy. METHODS: Aqueous humor was obtained during elective cataract surgery from T2DM patients with or without retinopathy and from healthy subjects. Reducing response was evaluated by MTT dye reduction and the generation of reactive oxygen species (ROS) was determined by chemiluminescence assay. Granulocytes were treated with phorbol dibutyrate (PDB)-stimulated. Cytokines were quantified by ELISA. RESULTS: Antioxidant capacity of aqueous humor from patients with retinopathy was greater (P<0.05) than that of healthy controls or persons with diabetes without retinopathy. ROS production in PDB (protein kinase C activator)-stimulated granulocytes from T2DM patients with or without retinopathy was inhibited by autologous aqueous humor. Concentrations of VEGF and IL-6 were similar in aqueous humor from healthy controls and from patients without retinopathy, but lower (P<0.05) than those from T2DM patients with retinopathy. Plasma levels of VEGF and IL-6 were similar (P>0.05) in healthy controls and in T2DM patients with and without retinopathy. CONCLUSION: Aqueous humor from T2DM patients with retinopathy exhibits elevated antioxidant activity with significant suppressive effect on ROS production and enhanced levels of locally secreted VEGF and IL-6 in comparison with T2DM patients without retinopathy. These results suggest an inflammatory profile in the absence of typical oxidative stress for T2DM patients with retinopathy, possibly resulting from the compensatory antioxidant response detected in the aqueous humor improving the ocular redox state.

High doses of in vitro beta-carotene, alpha-tocopherol and ascorbic acid induce oxidative stress and secretion of IL-6 in peripheral blood mononuclear cells from healthy donors.

BACKGROUND: Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species (ROS) and a biological system's ability to readily detoxify the reactive intermediates or repair the resulting damage. Our objective was to verify the existence of an in vitro dual effect of alpha-tocopherol, beta-carotene and ascorbic acid in peripheral blood mononuclear cells (PBMNC) of healthy donors and the inflammatory capacity by IL-6 production. METHODS: PBMNC were incubated with two concentrations of vitamin complex: [A] = Ascorbic Acid = 0.08µM, α- tocopherol = 0.04µM, ß-carotene = 0.0008 µM and [20A] = Ascorbic Acid = 1.6µM, α-tocopherol = 0.82µM, ß-carotene = 0.016µM. Oxidizing and reducing response were measured by chemiluminescence and MTT assays, respectively. IL-6 production was measured by sandwich ELISA. RESULTS: Ours results demonstrated that PBMNC (from 20-39-year-old donors) incubated with vitamins activated free radical production only in [20A] concentration. However, in the age groups of 40-59 and 60-80 years old, there was a significant reduction and activation of the oxidizing response with both concentrations, respectively. The inflammatory profile showed an elevation of IL-6 production in pro-oxidant and a decrease in antioxidant conditions. Correlation between ROS production and IL-6 releasing was observed. CONCLUSIONS: With this experiment we concluded that vitamins can exert an antioxidant effect and a pro-oxidant effect according to their concentration, and could be an inductor of an inflammatory process in vitro generating severe complications to the body in cellular levels.

HMGB1, TLR and RAGE: a functional tripod that leads to diabetic inflammation.

INTRODUCTION: Despite advances in treatment of diabetes mellitus, its prevalence continues to rise globally. Medications available are unable to control the vascular complications. Proposals for new therapeutic targets must take into account the hyperglycemia-induced signaling pathways that give rise to the inflammatory profile of the disease. AREAS COVERED: How high-mobility-group box-1 (HMGB1) protein, acting as an activator of Toll-like receptors (TLR) and receptors for advanced glycation end products (RAGE), creates a functional tripod that contributes to increased production of pro-inflammatory mediators, and sustains the chronic inflammatory state associated with diabetes. The interaction of TLR2 and TRL4 with host-derived ligands, which links diabetic complications with the innate immune response, and the activation of RAGE, which induces a cascade of metabolic responses, leading to the production and secretion of pro-inflammatory cytokines. EXPERT OPINION: Considering the involvement of the innate immune system, in association with the role of HMGB1 as an activator of TLR and RAGE, diabetes should be considered and treated as a metabolic and immunological disease, triggered by hyperglycemia. HMGB1 plays a central role in mediating injury and inflammation, and interactions involving HMGB1-TLR-RAGE constitute a tripod that trigger NF-κB activation. Blockade or downregulation of HMGB1, and/or control of the inflammatory tripod, represent a promising therapeutic approach for the treatment of diabetes.

cAMP activates the generation of reactive oxygen species and inhibits the secretion of IL-6 in peripheral blood mononuclear cells from type 2 diabetic patients.

Peripheral blood mononuclear cells (PBMNC) from patients with type 2 diabetes (DM2) have generated higher levels of reactive oxygen species (ROS) that were higher than those in cells from healthy individuals. In the presence of a cAMP-elevating agent, ROS production was significantly activated in PBMNC from DM2 patients but it was inhibited in cells from healthy subjects. Higher levels of IL-6 has been detected in the supernatant of PBMNC cultures from DM2 patients in comparison with healthy controls. When cells were cultured in the presence of a cAMP-elevating agent, the level of IL-6 decreased has by 46% in the supernatant of PBMNC from DM2 patients but it remained unaltered in controls. No correlations between ROS and IL-6 levels in PBMNC from DM2 patients or controls have been observed. Secretions of IL-4 or IFNgamma by PBMNC from patients or controls have not been affected by the elevation of cAMP. cAMP elevating agents have activated the production of harmful reactive oxidant down modulated IL-6 secretion by these cells from DM2 patients, suggesting an alteration in the metabolic response possibly due to hyperglicemia. The results suggest that cAMP may play an important role in the pathogenesis of diabetes.

[Oxidative stress: a review on metabolic signaling in type 1 diabetes]. / Estresse oxidativo: revisão da sinalização metabólica no diabetes tipo 1.

Diabetic complications appear to be multifactorial process. The biochemical and pathological mechanisms are associated with chronic hyperglycemia of diabetes and the increased oxidative stress which has been postulated to play a central role in these disorders. Accumulating evidence suggests that oxidative cell injury caused by free radicals contributes to the development of type 1 diabetes (DM1) complications and decreased efficiency of antioxidant defenses (both enzymatic and nonenzymatic) seems to correlate with the severity of pathological tissue changes in DM1. In this review, we report as oxidative stress may exert deleterious effects in diabetes, as well as address current strategies in study to down-regulating vascular injury.

Oxidizing and reducing responses in type 1 diabetic patients determined up to 5 years after the clinical onset of the disease.

Oxidative stress has been suggested to be the mediator of hyperglycaemia-induced diabetic complications. For this study we asked whether a significant imbalance between oxidizing and plasmatic reducing responses could be observed in DM1 patients receiving intensive therapy up to 5 years following the clinical onset of the disease. A total of 16 type 1 diabetic patients (DM1) without complications and 13 non-diabetic subjects were enrolled. Clinical and biochemical parameters were compared in the two populations studied. Moreover, reactive oxygen species (ROS) generation by granulocytes and the total plasma antioxidant status were simultaneously evaluated. Granulocytes-ROS derived and plasma antioxidant status were determined by chemiluminescence assay and tetrazolium dye reduction, respectively. Type 1 diabetic patients were receiving intensive therapy by multiple daily injections. In comparison with healthy individuals, DM1 patients exhibited an increase in ROS generation whilst plasma antioxidant status was unaltered and appeared to be sufficient to prevent the onset of typical oxidative stress. The clinical characteristics and the remaining biochemical parameters studied were similar for the two groups, except for a significantly decreased plasmatic level of uric acid in DM1 patients. This study suggests that the absence of complications in DM1 patients up to 5 years after onset of the disease may be associated with the oxidizing and reducing balance which need to be maintained in order to prevent or delay the onset of oxidative stress. The effective diabetic control involves evaluation of the oxidizing/antioxidant balance besides glycaemic control.

Estresse oxidativo: revisão da sinalização metabólica no diabetes tipo 1 / Oxidative stress: a review on metabolic signaling in type 1 diabetes

O diabetes melito e suas complicações apresentam origem multifatorial. Mecanismos bioquímicos e patológicos estão associados com hiperglicemia crônica no diabetes e o aumento do estresse oxidativo tem sido postulado com papel central nestas desordens. Evidências sugerem que a lesão celular oxidativa causada pelos radicais livres contribuem para o desenvolvimento das complicações no diabetes tipo 1 (DM1) e a diminuição das defesas antioxidantes (enzimáticas e não-enzimáticas) parecem correlacionar-se com a gravidade das alterações patológicas no DM1. Nesta revisão, relata-se como o estresse oxidativo pode exercer efeitos deletérios no diabetes e são apresentadas as opções terapêuticas em estudo para modulação da injúria vascular.

Diabetic complications appear to be multifactorial process. The biochemical and pathological mechanisms are associated with chronic hyperglycemia of diabetes and the increased oxidative stress which has been postulated to play a central role in these disorders. Accumulating evidence suggests that oxidative cell injury caused by free radicals contributes to the development of type 1 diabetes (DM1) complications and decreased efficiency of antioxidant defenses (both enzymatic and nonenzymatic) seems to correlate with the severity of pathological tissue changes in DM1. In this review, we report as oxidative stress may exert deleterious effects in diabetes, as well as address current strategies in study to down-regulating vascular injury.