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1.
Biotech Histochem ; 95(1): 8-17, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31264480

RESUMO

We investigated the effects of exercise in multiple sessions on anxiety- and depression-like behavior during aging, and the role of serotonin and serotonin 1A receptors in this process. Both 24-month-old (aged) and 6-month-old (adult) female rats were divided into five groups; aged control, adult control, aged + serotonin re-uptake inhibitors (SSRIs), aged + exercise, and aged + SSRIs + exercise. After exercise, all groups were evaluated using the open field arena, elevated plus maze and forced swim tests. We assessed serum corticosterone levels; number of amygdala, hippocampus and prefrontal cortex cells; tissue serotonin and serotonin 1A (5-HT1A) levels. In the open field test, aged rats exhibited a significant increase in locomotor activity compared to the SSRIs and SSRIs + exercise groups. During the elevated plus maze test, aged rats were observed less frequently in the open arms of assembly compared to adults. The duration increased in the exercise group and remained unchanged in the SSRIs group. In the forced swim test, the aged rats were more immobile compared to adults; no change was observed in the immobility time between these groups. The tissue serotonin levels in amygdala and hippocampus were higher in SSRIs + exercise group compared to the aged, exercised and SSRIs groups. The number of cells in the hippocampus, prefrontal cortex and amygdala decreased in the aged group compared to adult rats; increased numbers of cell were observed in exercise, SSRIs and SSRIs + exercise groups compared to aged rats. Exercise in multiple sessions may increase the number of cells in the hippocampus, prefrontal cortex and amygdala, which may reduce senile anxiety and depression. Also, serotonin and serotonin 1A receptors may play role in depression-like behavior.


Assuntos
Envelhecimento , Ansiedade , Depressão , Condicionamento Físico Animal , Tonsila do Cerebelo/citologia , Tonsila do Cerebelo/fisiologia , Animais , Ansiedade/prevenção & controle , Depressão/prevenção & controle , Feminino , Hipocampo/citologia , Hipocampo/fisiologia , Córtex Pré-Frontal/citologia , Córtex Pré-Frontal/fisiologia , Distribuição Aleatória , Ratos , Ratos Wistar , Receptor 5-HT1A de Serotonina/metabolismo , Serotonina/metabolismo , Inibidores Seletivos de Recaptação de Serotonina/administração & dosagem
2.
Physiol Int ; 104(1): 52-63, 2017 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-28361576

RESUMO

Objective Hepcidin may be an important mediator in exercise-induced iron deficiency. Despite the studies investigating acute exercise effects on hepcidin and markers of iron metabolism, we found no studies examining the chronic effects of walking exercises (WE) on hepcidin and markers of iron metabolism in premenopausal women. The chronic effects of two 8-week different-intensity WE on hepcidin, interleukin 6 (IL-6), and markers of iron metabolism in pre-menopausal women were examined. Methods Exercise groups (EG) [moderate tempo walking group (MTWG), n = 11; brisk walking group (BWG), n = 11] walked 3 days/week, starting from 30 to 51 min. Control group (CG; n = 8) did not perform any exercises. BWG walked at ∼70%-75%; MTWG at ∼50%-55% of HRRmax. VO2max, hepcidin, IL-6, and iron metabolism markers were determined before and after the intervention. Results VO2max increased in both EGs, favoring the BWG. Hepcidin increased in the BWG (p < 0.01) and CG (p < 0.05). IL-6 decreased in the BWG and the MTWG (p < 0.05; p < 0.01). While iron, ferritin, transferrin, and transferrin saturation levels did not change in any group, total iron binding capacity (p < 0.05), red blood cells (p < 0.05), and hematocrit (p < 0.01) increased only in the BWG. Conclusion Both WE types may be useful to prevent inflammation. However, brisk walking is advisable due to the positive changes in VO2max and some iron metabolism parameters, which may contribute to prevent iron deficiency. The increase in hepcidin levels remains unclear and necessitates further studies.


Assuntos
Exercício Físico/fisiologia , Hepcidinas/sangue , Mediadores da Inflamação/sangue , Interleucina-6/sangue , Ferro/sangue , Pré-Menopausa/sangue , Caminhada , Adulto , Biomarcadores/sangue , Feminino , Humanos , Pessoa de Meia-Idade , Consumo de Oxigênio , Fatores de Tempo
3.
Eur Rev Med Pharmacol Sci ; 20(8): 1642-55, 2016 04.
Artigo em Inglês | MEDLINE | ID: mdl-27160141

RESUMO

OBJECTIVE: Ischemia/reperfusion (I/R) injury is a major cause of acute organ dysfunction and I/R related acute renal failure is a common clinical problem. Diabetes mellitus is defined as a risk factor for the development of acute renal injury as diabetic nephropathy compromises the renal tolerance to ischemia. The aim of this study was to investigate the protective effect of magnesium sulfate in a diabetic rat renal I/R injury model. MATERIALS AND METHODS: Diabetes mellitus was induced using streptozotocin. Thirty-five rats were divided into five groups: Group I: Nondiabetic sham group; Group II: Diabetic sham group; Group III: Diabetic I/R group; Group IV: Diabetic I/R + prophylactic (preischemic) MgSO4; and Group V: Diabetic I/R + therapeutic (following reperfusion) MgSO4 group. MgSO4 was administered 200 mg/kg intraperitoneally. Renal I/R (45 min ischemia + 4 h reperfusion) was induced in both kidneys. Histomorphological, immunohistochemical (caspase-3 and iNOS) and biochemical (BUN, Creatinine) methods were performed to assess the blood and tissue samples. RESULTS: Histomorphological injury scores and immunostaining intensities (for both caspase-3 and iNOS) were significantly lower in the MgSO4 administered groups (prophylactic and therapeutic) than in the Diabetic IR group. There were no significant differences in biochemical parameters (BUN, Cr) between the MgSO4 administered groups and the Diabetic IR group. CONCLUSIONS: In the present study, it was demonstrated by histomorphological and immunohistochemical methods that magnesium sulfate administration before ischemia or following reperfusion significantly reduced renal I/R injury in a diabetic rat model.


Assuntos
Injúria Renal Aguda/prevenção & controle , Sulfato de Magnésio/uso terapêutico , Traumatismo por Reperfusão/prevenção & controle , Animais , Diabetes Mellitus Experimental , Rim/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Estreptozocina
4.
Biotech Histochem ; 90(1): 55-68, 2015 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-25203492

RESUMO

Regular treadmill running during adolescence improves learning and memory in rats. During adolescence, the baseline level of stress is thought to be greater than during other periods of life. We investigated the effects of voluntary and involuntary exercise on the prefrontal cortex and hippocampus, vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF) levels, and spatial learning, memory and anxiety in adolescent male and female rats. The voluntary exercise group was given free access to a running wheel for 6 weeks. The involuntary exercise group was forced to run on a treadmill for 30 min at 8 m/min 5 days/week for 6 weeks. Improved learning was demonstrated in both exercise groups compared to controls. Neuron density in the CA1 region of the hippocampus, dentate gyrus and prefrontal cortex were increased. Hippocampal VEGF and BDNF levels were increased in both exercise groups compared to controls. In females, anxiety and corticosterone levels were decreased; BDNF and VEGF levels were higher in the voluntary exercise group than in the involuntary exercise group. The adolescent hippocampus is affected favorably by regular exercise. Although no difference was found in anxiety levels as a result of involuntary exercise in males, females showed increased anxiety levels, and decreased VEGF and BDNF levels in the prefrontal cortex after involuntary exercise.


Assuntos
Ansiedade/metabolismo , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Cognição/fisiologia , Hipocampo/metabolismo , Fator A de Crescimento do Endotélio Vascular/metabolismo , Envelhecimento , Animais , Feminino , Aprendizagem/fisiologia , Masculino , Memória/fisiologia , Neurônios/metabolismo , Condicionamento Físico Animal , Córtex Pré-Frontal/metabolismo , Ratos Wistar
5.
Biotech Histochem ; 90(3): 206-15, 2015 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-25420894

RESUMO

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality during childhood. TBI enhances formation of reactive oxygen species that cause neuron damage and apoptosis. α-Lipoic acid (LA) is a free radical scavenger and biological antioxidant. We investigated the effects of LA treatment on the parietal and prefrontal cortex, and on the hippocampal regions of the brain in 7-day-old rat pups that had been subjected to contusion injury. Forty-two male rats were divided randomly into a control group, a TBI group and a TBI + LA treated group. LA was administered 30 min after TBI through an intragastric tube once daily for 2 days. Forty-eight hours after TBI, the animals were sacrificed and tissues were examined for apoptosis and density of neurons. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) and active caspase-3 immunostaining were used to detect apoptosis. Glutathione peroxidase (GPx), superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels also were measured. Histological evaluation showed that LA treatment significantly reduced TBI-induced neuronal death in the hippocampus, prefrontal and parietal cortex; TUNEL- and caspase-3-positive cells also were decreased in the same regions. In addition, LA administration increased GPx and SOD activity in the prefrontal cortex. It appears that LA may be beneficial for TBI in rats.


Assuntos
Antioxidantes/farmacologia , Lesões Encefálicas/tratamento farmacológico , Fármacos Neuroprotetores/farmacologia , Ácido Tióctico/farmacologia , Animais , Apoptose/efeitos dos fármacos , Encéfalo/patologia , Química Encefálica/efeitos dos fármacos , Lesões Encefálicas/metabolismo , Lesões Encefálicas/patologia , Marcação In Situ das Extremidades Cortadas , Masculino , Ratos , Ratos Wistar
6.
Biotech Histochem ; 89(5): 371-83, 2014 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-24476563

RESUMO

The developing brain is vulnerable to environmental factors. We investigated the effects of air that contained 0.05, 0.1 and 0.3% CO2 on the hippocampus, prefrontal cortex (PFC) and amygdala. We focused on the circuitry involved in the neurobiology of anxiety, spatial learning, memory, and on insulin-like growth factor-1 (IGF-1), which is known to play a role in early brain development in rats. Spatial learning and memory were impaired by exposure to 0.3% CO2 air, while exposure to 0.1 and 0.3% CO2 air elevated blood corticosterone levels, intensified anxiety behavior, increased superoxide dismutase (SOD) enzyme activity and MDA levels in hippocampus and PFC; glutathione peroxidase (GPx) enzyme activity decreased in the PFC with no associated change in the hippocampus. IGF-1 levels were decreased in the blood, PFC and hippocampus by exposure to both 0.1 and 0.3% CO2. In addition, apoptosis was increased, while cell numbers were decreased in the CA1 regions of hippocampus and PFC after 0.3% CO2 air exposure in adolescent rats. A positive correlation was found between the blood IGF-1 level and apoptosis in the PFC. We found that chronic exposure to 0.3% CO2 air decreased IGF-1 levels in the serum, hippocampus and PFC, and increased oxidative stress. These findings were associated with increased anxiety behavior, and impaired memory and learning.


Assuntos
Encéfalo/efeitos dos fármacos , Dióxido de Carbono/toxicidade , Poluentes Atmosféricos/toxicidade , Animais , Análise Química do Sangue , Encéfalo/crescimento & desenvolvimento , Feminino , Hipocampo/química , Hipocampo/efeitos dos fármacos , Fator de Crescimento Insulin-Like I/química , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Córtex Pré-Frontal/química , Córtex Pré-Frontal/efeitos dos fármacos , Ratos , Ratos Wistar
7.
Biotech Histochem ; 89(2): 126-35, 2014 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-24050191

RESUMO

It is known that regular aerobic exercise enhances cognitive functions and increases blood insulin-like growth factor 1 (IGF-1) levels. People living in urban areas spend most of their time indoors and indoor air quality can affect health. We investigated the effects of aerobic exercise in poor and good air quality environments on hippocampus and prefrontal cortex (PFC) neurons, anxiety, and spatial learning and memory in adolescent mice. Poor air quality impaired spatial learning and memory; exercise did not affect learning or memory impairment. Exercise in a good air quality environment improved spatial learning and memory. Poor air quality increased apoptosis in the hippocampus and PFC. Both exercised and sedentary groups living in a poor air quality environment had lower serum IGF-1 levels than those living in a good air quality environment. Living in a poor air quality environment has negative effects on the hippocampus, PFC and blood IGF-1 levels in adolescent mice, but exercise did not alter the negative effects of poor air quality.


Assuntos
Poluição do Ar em Ambientes Fechados , Fator de Crescimento Insulin-Like I/análise , Aprendizagem/fisiologia , Memória/fisiologia , Condicionamento Físico Animal , Animais , Análise Química do Sangue , Hipocampo/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Córtex Pré-Frontal/metabolismo
8.
Biotech Histochem ; 89(3): 161-71, 2014 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-24007473

RESUMO

Anxiety and depression are common in diabetics. Diabetes also may cause reduced leptin levels in the blood. We investigated the relation between diabetes induced anxiety- and depression-like behavior, and leptin and leptin receptor expression levels in diabetic rats. The anxiety- and depression-like behaviors of rats were assessed 4 weeks after intraperitoneal injection of streptozotocin. Diabetic rats exhibited greater anxiety-like behavior; they spent more time in closed branches of the elevated plus maze test and less time in the center cells of the open field arena. Increased depression-like behavior was observed in diabetic rats using the Porsolt swim test. Prefrontal cortex (PFC), blood leptin levels and PFC neuron numbers were decreased, and leptin receptor expression and apoptosis were increased in diabetic rats. Blood corticosterone levels also were increased in diabetic rats. These results indicate that reduction of leptin up-regulates leptin receptor expression and may affect PFC neurons, which eventually triggers anxiety- and depression-like behaviors in diabetic rats.


Assuntos
Ansiedade/metabolismo , Comportamento Animal , Depressão/metabolismo , Diabetes Mellitus Experimental/metabolismo , Leptina/metabolismo , Córtex Pré-Frontal/metabolismo , Receptores para Leptina/metabolismo , Animais , Ansiedade/psicologia , Corticosterona/sangue , Depressão/psicologia , Modelos Animais de Doenças , Masculino , Neurônios/metabolismo , Ratos Wistar , Estreptozocina
9.
Biotech Histochem ; 88(5): 250-7, 2013 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-23480228

RESUMO

Traumatic brain injury (TBI) may cause neuropsychiatric problems, such as anxiety disorder, that have negative effects on cognitive functions and behavior. We investigated the effects of progesterone on traumatic brain injury induced anxiety in 7-day-old rat pups subjected to contusion injury. Progesterone treatment decreased TBI induced anxiety and serum corticosterone levels, and increased serum IGF-1 levels. Moreover, progesterone treatment increased amygdala, prefrontal cortex and hippocampal neuron density. We found a negative correlation between serum corticosterone levels and anxiety tests, and a positive correlation between serum IGF-1 levels and anxiety tests. In addition, progesterone treatment decreased serum corticosterone compared to the controls and sham. Our results indicate that single dose progesterone may be effective for treating anxiety caused by TBI.


Assuntos
Ansiedade/etiologia , Lesões Encefálicas/tratamento farmacológico , Corticosterona/sangue , Fator de Crescimento Insulin-Like I/metabolismo , Córtex Pré-Frontal/citologia , Envelhecimento , Tonsila do Cerebelo/citologia , Animais , Ansiedade/tratamento farmacológico , Lesões Encefálicas/complicações , Hipocampo/citologia , Fator de Crescimento Insulin-Like I/genética , Neurônios/citologia , Neurônios/fisiologia , Ratos
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