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This is the first report that deals with the effect of yerba mate (YM) and chlorogenic acid (CGA) consumption on blood total creatine phosphokinase (CPK), lactate and irisin levels after a detraining period. Healthy mice (n = 50) were randomly separated into the following experimental groups: SED = sedentary control; TRAIN = mice submitted to training (swimming) for 8 weeks; DETRAIN = mice submitted to training for four weeks and after submitted to detraining for four weeks; DETRAIN CGA = mice submitted to training for four weeks and after submitted to both detraining and standard CGA consumption for four weeks; DETRAIN YM = mice submitted to training for four weeks and after submitted to both detraining and consumption of roasted YM infusion for four weeks. No significant (p > 0.05) difference was found in relation to the lactate value. The DETRAIN CGA group had a lower CPK data when compared with the other groups. The DETRAIN YM group showed a lactate value slightly lower than that from DETRAIN CGA one. Blood irisin value had no statistical (p > 0.05) difference between studied groups. Irisin value in sedentary group had a value non-statistically (p > 0.05) significant when compared with the other groups after a detraining period. Therefore, CGA could decrease the protein catabolism via CPK inhibition during detraining. YM may maintain a part of the lipid mobilization during detraining, leading to the sparing of a fraction of the lactate. Keywords: Ylex paraguariensis, mice, detraining, CPK, lactate, irisin

Serotonin exerts a significant role in the mammalian central nervous system embryogenesis and brain ontogeny. Therefore, we investigate the effect of neonatal treatment of d-fenfluramine (d-FEN), a serotonin (5-HT) releaser, on the behavioral expression of adult male Swiss mice. For this purpose, we divided pregnant female Swiss mice into two groups (n = 6 each and ~35 g). Their offspring were treated with d-FEN (3 mg/kg, s.c.) from postnatal days (PND) 5 to 20. At PND 21, one male puppy of each litter was euthanized; the midbrain and the hippocampus were dissected for RNA analysis. At PND 70, the male offspring underwent a behavioral assessment in the open field, elevated plus-maze, light-dark box, tail suspension, and rotarod test. The programmed animals had a decrease in 5HT1a, serotonin transporter (SERT), and brain-derived neurotrophic factor (BDNF) expression in the mesencephalic raphe region. Alternatively, there was a reduction only in the tryptophan hydroxylase (TPH2) and BDNF expression in the hippocampus. In the light-dark box test, offspring of the treated group had higher latency to light and less time on the light side than the control. Also, it was observed less time of immobility in the tail suspension test. We also observed low motor skill learning in the rotarod test. These findings suggest that programming with d-FEN during the neonatal period alters a mesencephalic and hippocampal serotonergic system, promoting anxiety, antidepressant behavior, low coordination, and motor learning in adults.

Evaluate the anti-inflammatory activity in vivo and in vitro of cis-(±)-acetate of 4-chloro-6-(naphtalene-1-yl)-tetrahydro-2H-pyran-2-yl) methyl 2-(2-(2,6-diclorofenylamine) phenyl (LS19). Male Swiss mice were analyzed in the paw edema, ear edema, and air pouch tests, and in vitro COX inhibition, cytotoxicity evaluation, and cytokine and nitric oxide determination tests. The compound showed effect on the carrageenan- and bradykinin-induced paw edema and capsaicin-induced ear edema tests. In addition, the compound was able to inhibit leukocyte migration to decrease the levels of the pro-inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) and to increase the levels of the anti-inflammatory cytokine IL-10. The compound was also able to reduce levels of TNF-α, IL-6, and nitric oxide in the RAW 264.7 cell line and to inhibit COX activity. LS19 did not induce any significant changes in the viability of RAW 264.7 cells, demonstrating safety for these cell lines. The compound LS19 did not reduce the production of gastric mucus and induced a smaller increase in the extent of gastric lesions than that developed by the administration of diclofenac. In summary, the new compound proved to be safer and it had additional mechanisms compared to diclofenac.

The present study aimed to compare the exercise order of an acute bout of resistance exercise (RT) on acute thyroid hormonal responses. Eight (n = 8) healthy men were randomly separated into two experimental groups: A) the order from multi- to single-joint exercises (MJ-SJ) and B) the order from single- to multijoint exercises (SJ-MJ). For all exercises in both orders, the subjects were submitted to 3 sets of 10 repetitions, with rest intervals of 2 minutes between sets and 3 minutes between exercises. Blood samples were collected at rest and 0, 15, 30, 60 and 120 min after the end of the exercise session. In thyroidstimulating hormone (TSH), differences between groups (MJ-SJ < SJ-MJ) were observed within 15 minutes after the session. In 3,5,3′-triiodothyronine (T3), differences between groups were observed between 30 (MJ-SJ > SJ-MJ) and 120 minutes (MJ-SJ < SJ-MJ) after the session. In 3,5,3′,5′-tetraiodothyronine (T4), differences between groups (MJ-SJ > SJ-MJ) were observed within 15 minutes after the RT session. The order of RT exercises significantly changes the hormonal responses of TSH, T3 and T4. In addition, the exercise order should be chosen according to the individual’s objectives.

Introduction: Alzheimer disease’s (AD) is a neurodegenerative disorder and it is known that the central nervous system (CNS) is an important target of thyroid hormones (TH). Moreover, an inverse association between serum triiodothyronine (T3) levels and the risk of AD was reported. Aim: To evaluate the effects of T3 treatment on the depression-like behavior observed in male transgenic 3xTg-AD mice. Main methods: Animals were divided into 2 groups, one group received daily intraperitoneal injections of L-T3 (T3 group), and the other received an equivalent volume of 0.9% saline (Control group). The experimental protocol lasted 21 days, and behavioral tests were conducted on days 15-19. At the conclusion of the experiment, the TH profile and hippocampal gene expression were evaluated. Key findings: It was observed that the T3-treated group presented significantly increased serum T3 and decreased thyroxine (T4) levels. When compared to control hippocampal samples, the T3 group exhibited attenuated glycogen synthase kinase-3 (GSK3), metalloproteinase 10 (ADAM10), amyloid-beta precursor-protein (APP), serotonin transporter (SERT), 5HT1a receptor, monocarboxylate transporter 8 (MCT8) and bone morphogenetic protein 7 (BMP-7) gene expression levels and augmented superoxide dismutase 2 (SOD2) and Hairless gene expression levels. Additionally, T3-treated animals displayed reduced immobility time in both the tail suspension and forced swim tests, and in the latter presented a higher latency time when compared to the control group. Significance: Taken together, our results demonstrate that in an AD mouse model, T3 supplementation promotes improvements in depression-like behavior, likely through the modulation of the serotonergic pathway, and also attenuated disease progression.

Alzheimer disease's (AD) is a neurodegenerative disorder characterized by cognitive and behavioral impairment. The central nervous system is an important target of thyroid hormones (TH). An inverse association between serum triiodothyronine (T3) levels and the risk of AD symptoms and progression has been reported. We investigated the effects of T3 treatment on the depression-like behavior in male transgenic 3xTg-AD mice. Animals were divided into 2 groups treated with daily intraperitoneal injections of 20 ng/g of body weight (b.w.) L-T3 (T3 group) or saline (vehicle, control group). The experimental protocol lasted 21 days, and behavioral tests were conducted on days 18-20. At the end of the experiment, the TH profile and hippocampal gene expression were evaluated. The T3-treated group significantly increased serum T3 and decreased thyroxine (T4) levels. When compared to control hippocampal samples, the T3 group exhibited attenuated glycogen synthase kinase-3 (GSK3), metalloproteinase 10 (ADAM10), amyloid-beta precursor-protein (APP), serotonin transporter (SERT), 5HT1A receptor, monocarboxylate transporter 8 (MCT8) and bone morphogenetic protein 7 (BMP-7) gene expression, whereas augmented superoxide dismutase 2 (SOD2) and Hairless gene expression. T3-treated animals also displayed reduced immobility time in both the tail suspension and forced swim tests, and in the latter presented a higher latency time compared to the control group. Therefore, our findings suggest that in an AD mouse model, T3 supplementation promotes improvements in depression-like behavior, through the modulation of the serotonergic related genes involved in the transmission mediated by 5HT1A receptors and serotonin reuptake, and attenuated disease progression.