Influência do exercício físico na prevenção de alterações no status oxidativo, metabolismo energético e mecânica respiratória observadas em ratos submetidos à lesão pulmonar

A síndrome da angustia respiratória é caracterizada por uma inflamação bilateral, infiltrado intersticial e insuficiência respiratória. Acredita-se que o exercício físico seja benéfico na prevenção de doenças pulmonares. O objetivo deste estudo foi avaliar os efeitos do exercício físico sobre alguns parâmetros de estresse oxidativo, metabolismo energético e alterações na mecânica respiratória (complacência, elastância e resistência do sistema respiratório) no pulmão de ratos submetidos à lesão pulmonar. O efeito protetor do exercício físico também foi avaliado sobre às alterações da barreira alvéolo-capilar (contagem total de células, atividade da LDH e proteína total) e o conteúdo de fosfolipíedeos no lavado broncoalveolar, bem como sobre o infiltrado inflamatório e o edema no parênquima pulmonar. Os animais foram submetidos a dois meses de exercício físico moderado, realizado 3 vezes por semana. Transcorrido o período de exercício, a lesão pulmonar foi induzida através da injeção intratraqueal de LPS (100 g/100g de peso corporal) e doze horas após foram submetido à avaliação da mecânica respiratória e/ou foram mortos para a coleta do material. Foram avaliados parâmetros de estresse oxidativo [formação de espécies reativas, lipoperoxidação, dano oxidativo a proteínas, atividade de enzimas antioxidantes superóxido dismutase (SOD) catalase (CAT) glutationa peroxidase (GPX), níveis de nitritos, capacidade antioxidante total (TRAP), conteúdo de glutationa (GSH)] e fator nuclear kappabeta (NF-кβ/p65) no pulmão de ratos submetidos à lesão pulmonar Parâmetros de metabolismo energético também foram avaliamos [succinato desidrogenase (SDH), complexo II e citocromo c oxidase e níveis de ATP]. Resultados mostraram um aumento nos níveis de espécies reativas, lipoperoxidação, danos a proteínas, níveis de nitritos, bem como no NF-кβ/p65 no pulmão de ratos submetidos a lesão pulmonar. O exercício físico foi capaz de prevenir o aumento das espécies reativas, os níveis de nitritos o NF-кβ/p65; e parcialmente preveniu o dano às proteínas. As atividades da SOD e CAT não foram alteradas nos animais submetidos à lesão pulmonar. No entanto, no grupo lesão pulmonar e exercício houve um aumento na atividade dessas enzimas. A atividade da GPX e G6PD, níveis de GSH e TRAP estão diminuídos nos animais submetidos à lesão pulmonar; o exercício preveniu totalmente tais alterações. Resultados mostraram que os animais submetidos à lesão pulmonar apresentaram uma diminuição na atividade das enzimas da cadeia transportadora de elétrons e nos níveis de ATP e formação de edema pulmonar. Também observamos uma redução da complacência pulmonar e um aumento da resistência alveolar. O exercício preveniu totalmente a diminuição nas atividades do complexo II e SDH e a formação do edema, bem como preveniu parcialmente a resistência alveolar. Ratos submetidos à lesão pulmonar aguda apresentaram um aumento na contagem total de células, na atividade da LDH nas proteínas e uma diminuição nos fosfolipídeos no lavado broncoalveolar; exercício preveniu parcialmente somente o aumento na atividade da LDH. Nossos achados sugerem que o exercício físico pode ter um importante papel na prevenção de algumas alterações presentes na lesão pulmonar.Acute respiratory distress syndrome is characterized by pulmonary inflammation, interstitial infiltrates and respiratory failure. It is believed that exercise is beneficial in preventing lung diseases. The objective of the present study was evaluated the effects of physical exercise on some parameters of oxidative stress, energy metabolism and respiratory mechanics (dynamic and static compliance, elastance and respiratory system resistance) in the lungs of rats submitted to lung injury. The protective effect of physical exercise was also evaluated with regard to the alterations in the alveolar-capillary barrier (total cell count, activity of LDH and total protein) and phospholipids content in the bronchoalveolar lavage, as well as on the inflammatory infiltration and edema in the pulmonary parenchyma. The animals were submitted to two months of moderate physical exercise three times per week. After this period of physical exercise, lung injury was induced by intratracheal instillation of LPS (100g/100g body weight) and twelve hours after the injury were performed the respiratory mechanical and/or were killed and collected material. It was evaluated oxidative stress parameters [formation of reactive species, lipid peroxidation, oxidative damage to protein, antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), nitrite levels, total antioxidant capacity (TRAP), glutathione content (GSH)] and nuclear factor-kappa Beta (NF-кβ/p65) in lung of rats submitted to lung injury. Parameters of energy metabolism were also evaluating [succinate dehydrogenase (SDH), complex II and cytochrome c oxidase, and ATP levels]. Results showed an increase in reactive species production, lipid peroxidation, oxidative damage to protein, as well as nitrite levels, as well NF-кβ/p65 in lung of rats submitted to lung injury. Physical exercise was able to totally prevent the increase in reactive species, nitrite levels and NF-кβ/p65, but partially prevented the damage to protein. The activities of SOD and CAT were not changed in animals submitted to lung injury. However in exercise–lung injury rats group the activities of these enzymes were increased. The activity of GPx, GSH content and TRAP were decreased in lung of rats submitted to lung injury. Physical exercise totally prevented such effects. Results showed that rats subjected to lung injury presented a decrease in activities of the enzymes of the electron transport chain and ATP levels as well as presented the pulmonary edema formation. It was also observed decreased lung dynamic and static compliance and increased in respiratory system resistance. Physical exercise was able to totally prevent the decrease in SDH and complex II activities and the pulmonary edema formation, as well partially prevented the respiratory system resistance. Rats subjected to lung injury presented an increase in total cell, activity of LDH, total protein and phospholipids content in bronchoalveolar lavage; exercise only partially prevented the increase in the activity of LDH. Our findings suggest that exercise may have an important role as protector in some alterations presents in lung injury

Functional electrical stimulation for foot drop in post-stroke people: quantitative effects on step-to-step symmetry of gait using a wearable inertial sensor

The main purpose of the present study was to assess the effects of foot drop stimulators (FDS) in individuals with stroke by means of spatio-temporal and step-to-step symmetry, harmonic ratio (HR), parameters obtained from trunk accelerations acquired using a wearable inertial sensor. Thirty-two patients (age: 56.84 ± 9.10 years; 68.8% male) underwent an instrumental gait analysis, performed using a wearable inertial sensor before and a day after the 10-session treatment (PRE and POST sessions). The treatment consisted of 10 sessions of 20 min of walking on a treadmill while using the FDS device. The spatio-temporal parameters and the HR in the anteroposterior (AP), vertical (V), and mediolateral (ML) directions were computed from trunk acceleration data. The results showed that time had a significant effect on the spatio-temporal parameters; in particular, a significant increase in gait speed was detected. Regarding the HRs, the HR in the ML direction was found to have significantly increased (+20%), while those in the AP and V directions decreased (approximately 13%). Even if further studies are necessary, from these results, the HR seems to provide additional information on gait patterns with respect to the traditional spatio-temporal parameters, advancing the assessment of the effects of FDS devices in stroke patients

Influência do exercício físico na prevenção de alterações no status oxidativo, metabolismo energético e mecânica respiratória observadas em ratos submetidos à lesão pulmonar

A síndrome da angustia respiratória é caracterizada por uma inflamação bilateral, infiltrado intersticial e insuficiência respiratória. Acredita-se que o exercício físico seja benéfico na prevenção de doenças pulmonares. O objetivo deste estudo foi avaliar os efeitos do exercício físico sobre alguns parâmetros de estresse oxidativo, metabolismo energético e alterações na mecânica respiratória (complacência, elastância e resistência do sistema respiratório) no pulmão de ratos submetidos à lesão pulmonar. O efeito protetor do exercício físico também foi avaliado sobre às alterações da barreira alvéolo-capilar (contagem total de células, atividade da LDH e proteína total) e o conteúdo de fosfolipíedeos no lavado broncoalveolar, bem como sobre o infiltrado inflamatório e o edema no parênquima pulmonar. Os animais foram submetidos a dois meses de exercício físico moderado, realizado 3 vezes por semana. Transcorrido o período de exercício, a lesão pulmonar foi induzida através da injeção intratraqueal de LPS (100 g/100g de peso corporal) e doze horas após foram submetido à avaliação da mecânica respiratória e/ou foram mortos para a coleta do material. Foram avaliados parâmetros de estresse oxidativo [formação de espécies reativas, lipoperoxidação, dano oxidativo a proteínas, atividade de enzimas antioxidantes superóxido dismutase (SOD) catalase (CAT) glutationa peroxidase (GPX), níveis de nitritos, capacidade antioxidante total (TRAP), conteúdo de glutationa (GSH)] e fator nuclear kappabeta (NF-кβ/p65) no pulmão de ratos submetidos à lesão pulmonar Parâmetros de metabolismo energético também foram avaliamos [succinato desidrogenase (SDH), complexo II e citocromo c oxidase e níveis de ATP]. Resultados mostraram um aumento nos níveis de espécies reativas, lipoperoxidação, danos a proteínas, níveis de nitritos, bem como no NF-кβ/p65 no pulmão de ratos submetidos a lesão pulmonar. O exercício físico foi capaz de prevenir o aumento das espécies reativas, os níveis de nitritos o NF-кβ/p65; e parcialmente preveniu o dano às proteínas. As atividades da SOD e CAT não foram alteradas nos animais submetidos à lesão pulmonar. No entanto, no grupo lesão pulmonar e exercício houve um aumento na atividade dessas enzimas. A atividade da GPX e G6PD, níveis de GSH e TRAP estão diminuídos nos animais submetidos à lesão pulmonar; o exercício preveniu totalmente tais alterações. Resultados mostraram que os animais submetidos à lesão pulmonar apresentaram uma diminuição na atividade das enzimas da cadeia transportadora de elétrons e nos níveis de ATP e formação de edema pulmonar. Também observamos uma redução da complacência pulmonar e um aumento da resistência alveolar O exercício preveniu totalmente a diminuição nas atividades do complexo II e SDH e a formação do edema, bem como preveniu parcialmente a resistência alveolar. Ratos submetidos à lesão pulmonar aguda apresentaram um aumento na contagem total de células, na atividade da LDH nas proteínas e uma diminuição nos fosfolipídeos no lavado broncoalveolar; exercício preveniu parcialmente somente o aumento na atividade da LDH. Nossos achados sugerem que o exercício físico pode ter um importante papel na prevenção de algumas alterações presentes na lesão pulmonar.Acute respiratory distress syndrome is characterized by pulmonary inflammation, interstitial infiltrates and respiratory failure. It is believed that exercise is beneficial in preventing lung diseases. The objective of the present study was evaluated the effects of physical exercise on some parameters of oxidative stress, energy metabolism and respiratory mechanics (dynamic and static compliance, elastance and respiratory system resistance) in the lungs of rats submitted to lung injury. The protective effect of physical exercise was also evaluated with regard to the alterations in the alveolar-capillary barrier (total cell count, activity of LDH and total protein) and phospholipids content in the bronchoalveolar lavage, as well as on the inflammatory infiltration and edema in the pulmonary parenchyma. The animals were submitted to two months of moderate physical exercise three times per week. After this period of physical exercise, lung injury was induced by intratracheal instillation of LPS (100g/100g body weight) and twelve hours after the injury were performed the respiratory mechanical and/or were killed and collected material. It was evaluated oxidative stress parameters [formation of reactive species, lipid peroxidation, oxidative damage to protein, antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), nitrite levels, total antioxidant capacity (TRAP), glutathione content (GSH)] and nuclear factor-kappa Beta (NF-кβ/p65) in lung of rats submitted to lung injury Parameters of energy metabolism were also evaluating [succinate dehydrogenase (SDH), complex II and cytochrome c oxidase, and ATP levels]. Results showed an increase in reactive species production, lipid peroxidation, oxidative damage to protein, as well as nitrite levels, as well NF-кβ/p65 in lung of rats submitted to lung injury. Physical exercise was able to totally prevent the increase in reactive species, nitrite levels and NF-кβ/p65, but partially prevented the damage to protein. The activities of SOD and CAT were not changed in animals submitted to lung injury. However in exercise–lung injury rats group the activities of these enzymes were increased. The activity of GPx, GSH content and TRAP were decreased in lung of rats submitted to lung injury. Physical exercise totally prevented such effects. Results showed that rats subjected to lung injury presented a decrease in activities of the enzymes of the electron transport chain and ATP levels as well as presented the pulmonary edema formation. It was also observed decreased lung dynamic and static compliance and increased in respiratory system resistance. Physical exercise was able to totally prevent the decrease in SDH and complex II activities and the pulmonary edema formation, as well partially prevented the respiratory system resistance. Rats subjected to lung injury presented an increase in total cell, activity of LDH, total protein and phospholipids content in bronchoalveolar lavage; exercise only partially prevented the increase in the activity of LDH. Our findings suggest that exercise may have an important role as protector in some alterations presents in lung injury

Bicephalic Transcranial Direct-Current Stimulation Does Not Add Benefits to a Footdrop Stimulator for Improving Functional Mobility in People with Chronic Hemiparesis after Stroke: a Double-Blind, Randomized Controlled Trial

The aim of this study was to assess the effects of applying transcranial direct-current stimulation (tDCS), a footdrop stimulator (FDS), and gait training simultaneously on functional mobility in people with chronic hemiparesis after stroke

Experimental lung injury promotes changes in oxidative/nitrative status and inflammatory markers in cerebral cortex of rats

In the present study, we investigate the effect of lung injury on parameters of oxidative/nitrative stress [reactive oxygen species production, nitrite levels, thiobarbituric acid-reactive substances (TBARS), carbonyl content, sulfhydryl content, activities of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase), total radical-trapping antioxidant potential, glutathione content, and glucose-6-phosphate dehydrogenase], as well as on inflammation mediators [immunocontent of nuclear factor-kappaB (NF-κB) total (p65), NF-κB phosphorylated (pp65) subunit (cytosolic and nuclear), TNF-α, IL-1β, IL-6, and IL-10] in the cerebral cortex. Cytokine levels in serum were also evaluated. Adult Wistar rats were submitted to lung injury induced by intratracheal instillation of lipopolysaccharide in a dose of 100 μg/100 g body weight. Sham group (control) received isotonic saline instillation. Twelve hours after the injury, rats were decapitated and blood samples were collected and the cerebral cortex dissected out. Results showed an increase in reactive oxygen species production, TBARS, and nitrite and carbonyl levels in the cerebral cortex of rats submitted to lung injury. Antioxidant enzymatic defenses were altered, superoxide dismutase and glutathione peroxidase activities decreased, and catalase activity increased. Non-enzymatic antioxidant capacity, glutathione content, and glucose-6-phosphate dehydrogenase were decreased. Inflammatory parameters were also altered in the cerebral cortex of rats subjected to lung injury; it was observed an increase in the immunocontent of NF-κB/p65 (nuclear fraction) and NF-κB/pp65 (cytosolic and nuclear faction), as well as an increase in TNF-α, IL-1β, IL-6, and IL-10 levels. The levels of IL-10 also increased in the serum. Our findings show that the lung injury alters oxidative/nitrative status and induces inflammation in the cerebral cortex of rats, which might be associated with cognitive impairments present in patients with lung injury

Chronic methylphenidate administration alters antioxidant defenses and butyrylcholinesterase activity in blood of juvenile rats

Methylphenidate (MPH), a psychostimulant that affects both dopaminergic and noradrenergic systems, is one of the most frequently prescribed treatments for attention-deficit hyperactivity disorder. The present study investigated the effects of chronic administration of MPH on some parameters of oxidative stress, as well as on butyrylcholinesterase (BuChE) activity in blood of young rats. Rats received intraperitoneal injections of MPH (2.0 mg/kg) once a day, from the 15th to the 45th day of age or an equivalent volume of 0.9% saline solution (controls). Two hours after the last injection, animals were euthanized, and blood was collected. Results demonstrated that MPH did not alter the dichlorofluorescein formed, decreased both thiobarbituric acid reactive substances and total non-enzymatic radical-trapping antioxidant, and increased superoxide dismutase and catalase activities, suggesting that this psychostimulant may alter antioxidant defenses. BuChE activity was increased in blood of juvenile rats subjected to chronic MPH administration. These findings suggest that MPH may promote peripheral oxidative adaptations and cholinergic changes