Analú Bender Dos Santos

Exercise Training under Exposure to Low Levels of Fine Particulate Matter: Effects on Heart Oxidative Stress and Extra-to-Intracellular HSP70 Ratio

Fine particulate matter (PM2.5) promotes heart oxidative stress (OS) and evokes anti-inflammatory responses observed by increased intracellular 70 kDa heat shock proteins (iHSP70). Furthermore, PM2.5 increases the levels of these proteins in extracellular fluids (eHSP70), which have proinflammatory roles. We investigated whether moderate and high intensity training under exposure to low levels of PM2.5 modifies heart OS and the eHSP70 to iHSP70 ratio (H-index), a biomarker of inflammatory status. Male mice (n = 32), 30 days old, were divided into six groups for 12 weeks: control (CON), moderate (MIT) and high intensity training (HIT), exposure to 5 μg of PM2.5 daily (PM2.5), and moderate and high intensity training exposed to PM2.5 (MIT + PM2.5 and HIT + PM2.5 groups). The CON and PM2.5 groups remained sedentary. The MIT + PM2.5 group showed higher heart lipid peroxidation levels than the MIT and PM2.5 groups. HIT and HIT + PM2.5 showed higher heart lipid peroxidation levels and lower eHSP70 and H-index levels compared to sedentary animals. No alterations were found in heart antioxidant enzyme activity or iHSP70 levels. Moderate exercise training under exposure to low levels of PM2.5 induces heart OS but does not modify eHSP70 to iHSP70 ratio (H-index). High intensity exercise training promotes anti-inflammatory profile despite exposure to low levels of PM2.5.

Efeitos do tratamento com glutamina via enteral em modelo animal de sepse

The aim of study was to evaluate the effects of enteral glutamine treatment on clinical parameters in an animal model of sepsis. Were used 24 mice (B6129SF2/J) in two experiments: First 11 mice were divided into three groups to evaluate the animal model better to simulate the sepsis. Animals received saline (control) or faecal solution 10 or 20% (i.p), and were evaluated glycaemia and rectal temperature for 24h. Second 13 mice were divided into: Control, Sepsis, Glutamine and Sepsis+Glutamine. Glutamine was administered by gavage (1 g/kg) each 4h for 47h. Glycaemia, rectal temperature, leukocyte count and body weight was evaluated. Results: The administration of 20% faecal solution induced hypodynamic phase of sepsis with hypothermia, hypoglycaemia and low leukocyte count. The treatment with glutamine avoids the decrease in leukocyte. Conclusion: Since the immune response is essential in sepsis, the use of glutamine can be useful as adjuvant therapy in sepsis.

Characterization of Schinus lentiscifolius March (Anacardiaceae) Bark Extract and its Effects on Lymphocyte Oxidative Stress and Heat Shock Response

Schinus lentiscifolius Marchand has been used in folk medicine to treat immunoinflammatory related diseases, which are marked by OS and altered HSR. Our study aimed to evaluate OS and HSR in lymphocytes treated with S. lentiscifolius bark extracts. S. lentiscifolius barks were partitioned with solvents to obtain hexane (SL‐HEX), ethyl acetate (SL‐ACOET) and methanol (SL‐MEOH) extracts, and the presence of bioactive compounds was evaluated by thin layer chromatography. Total phenols were measured by the Folin–Ciocalteu method and flavonoids were identified by HPLC‐DAD‐ESI‐MS/MS. Antioxidant capacity was verified by DPPH method, cell viability by Trypan Blue method, lipid peroxidation by TBARS and HSP70 by immunoblotting. The SL‐ACOET extract presented higher content of phenolic compounds and antioxidant activity in vitro. It was able to reduce lipid peroxidation levels in lymphocytes induced by H2O2 and improved cell viability. The SL‐ACOET extract inhibited HSR by a decrease in both intracellular content and release of 70 kDa heat shock proteins (HSP70) and also by decrease extra‐to‐intracellular HSP70 ratio in lymphocytes submitted to heat shock (2 h, 41 °C). S. lentiscifolius bark extract has antioxidant activity and inhibitory effect on HSR probably due to the presence of polyphenols as the flavonoids quercetin and kaempferol.

Lifestyle and Aging Effects in the Development of Insulin Resistance — Activating the Muscle as Strategy Against Insulin Resistance by Modulating Cytokines and HSP70

This chapter discusses about subclinical processes related to insulin resistance development that worsen the muscle metabolic functions, generated by factors such as lifestyle (bad quality food intake and sedentary behavior) and aging. Also discussed are the effects of regular physical exercise as a strategy to prevent the metabolic impairment in organisms, approaching since muscle subclinical molecular processes to the whole body’s integrative physiology. Insulin resistance development includes modification in the pattern of inflammatory cytokines, heat shock proteins, tissuespecific defects in insulin action and signaling, oxidative stress and ectopic lipid deposition. The exercise is a known modulator of all parameters listed above and has important role in the regulation of “immune-metabolic” homeostasis from the muscle to the whole body. This chapter aims to present a new molecular approach related to the control of metabolism and encourage scientists and students to propose new strategies against insulin resistance and diabetes type 2 developments.

Exposure to particulate matter modifies the pancreas extracellular/intracellular HSP70 ratio in high-fat diet treated mice: a marker of the diabetes development risk.

Background Evidences highlights exposure to fine particulate matter (PM2.5) as a risk factor for development of type 2 diabetes (T2D), especially in high-fat diet (HFD) fed mice. Under stressful conditions, cells respond by synthesizing a suite of intracellular stress response proteins, that plays a fundamental protective role in metabolic disorders, the 70 kDa family of heat shock proteins (iHSP70). However, while iHSP70 presents anti-inflammatory proprieties, their extracellular levels (eHSP72), presents pro-inflammatory roles. We propose to investigate the effects of HFD+PM2.5 association in the HSP70 status, and this relation to the risk of developing T2D.