Navegando por Assunto "Bebidas alcoolicas - consumo"

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Acesso aberto (Open Access)
Atividade neuroprotetora do treinamento físico moderado contra os danos morfofuncionais cerebelares causados pelo consumo de etanol de forma intensa e episódica (Binge drinking) em ratos
(Universidade Federal do Pará, 2019-09) VIEIRA, Kátia Lamarão; LIMA, Rafael Rodrigues; http://lattes.cnpq.br/3512648574555468; https://orcid.org/0000-0003-1486-4013
Ethanol (EtOH) is a psychotropic drug, central nervous system (CNS) depressant, but widely encouraged and consumed by Brazilian society, as well as in much of the world, reflecting on a public health problem. In recent decades, teenagers have been practicing a very common practice, which is binge drinking. The harmful consumption of EtOH promotes, besides biopsychosocial alteration, the homeostatic imbalance that causes neurodegeneration and loss of function with motor disorders. In contrast, the practice of moderate physical training (MPT) has been recommended for the maintenance of physical and mental health, as well as prevention or minimization of the development of some diseases due to motor activity inducing plastic and dynamic changes in the CNS, in order to favor the neurogenesis, synaptogenesis and angiogenesis, besides contributing to the synaptic modulation. In view of the benefits of MPT, it was investigated the neuroprotective effects on motor, tissue and biochemical parameters in the cerebellum of rats exposed to binge-pattern EtOH from adolescence to adulthood. Forty male Wistar rats with 30 days old were used and divided into four groups, the control being sedentary animals and treated with distilled H2O; the trained, composed of animals exercised and treated with distilled H2O; EtOH, formed by sedentary animals and treated with doses of 3 g/kg/day EtOH, 20% (w/v); and Trained + EtOH, with exercised animals and treated with doses of 3 g/kg/day EtOH, 20% (w/v). The MPT protocol was performed on a rodent treadmill for 5 days for 4 weeks and binge-pattern EtOH doses were administered by intragastric gavage in the same weeks as the MPT. After this period, the animals were submitted to open field and beam walking behavioral tests. Then, they were euthanized for cerebellum collection, evaluating immunohistochemistry from the levels of trolox equivalent antioxidant capacity (TEAC), reduced glutathione (GSH), nitrite and lipid peroxidation (LPO); as well as Purkinje cell morphology (PC), the fraction of anti-synaptophysine (SYP) and anti-myelin basic protein (MBP) immunolabeled area. According to the result, EtOH caused severe oxidative stress and motor damage, but the execution of the MPT performed promoted neuroprotective effects in the rat cerebellum, among them, the modulation of oxidative biochemistry by the restoration of GSH levels. decreased LPO levels and increased TEAC, as well as preventing neuronal loss, synaptic vesicle damage (SYP) and myelin components (MBP). Therefore, MPT can be considered as a significant therapeutic strategy for the acquisition of redox homeostasis, avoiding oxidative biochemistry imbalance, as well as tissue and functional damage in the cerebellum of rats treated by binge pattern EtOH.
Acesso aberto (Open Access)
Investigação dos efeitos da cafeína e SCH58261 sobre as alterações comportamentais e no estresse oxidativo, e papel dos receptores A2A na potenciação de longo prazo após intoxicação por etanol em padrão binge em ratos fêmeas da adolescência a fase adulta
(Universidade Federal do Pará, 2022-11) PINHEIRO, Bruno Gonçalves; MAIA, Cristiane do Socorro Ferraz; http://lattes.cnpq.br/4835820645258101
Introduction: Binge consumption of ethanol is an intermittent and episodic pattern of ingestion involved in several brain disorders that affect adolescents, considered more susceptible to damage that persists into adulthood. In the deleterious effects of ethanol, an important intoxication mechanism is the overproduction of adenosine, which causes hyperexcitability in its receptors, generating behavioral changes and oxidative stress. These receptors are antagonized by caffeine, a bioactive compound that can modulate the deleterious overactivation of ethanol. Objective: The aim of this study was to investigate the effects of caffeine administration on behavioral changes related to locomotion, anxiety, cognition and oxidative balance induced by ethanol in the binge drinking pattern during adolescence. In addition, it aims to assess the contribution of A2A receptors in the observed changes, including long-term potentiation (LTP). Material and Methods: Female Wistar rats (35 days old; n = 102) were allocated into six groups: control (distilled water, v.o), ethanol (3 g/kg/day; 3 days on-4 days off, v.o) , caffeine (10 mg/kg/day, v.o), caffeine + ethanol, A2A antagonist SCH58261 (0.1 mg/kg/day, intraperitoneal - i,p) and ethanol + SCH58261. The animals were submitted to open field behavioral tests, object recognition and elevated plus maze. The oxidative biochemistry parameters of trolox equivalent antioxidant capacity (TEAC), glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), nitric oxide (NO), thiobarbituric acid reactive substances (TBARS) in the pre- frontal and hippocampus. LTP recordings in the medial prefrontal cortex (mPFC), ventral (vHip) and dorsal (dHIP) portions of the hippocampus of the control, ethanol, ethanol + SCH58261 and SCH58261 groups were evaluated through electrophysiology. Results: Caffeine prevented ethanol-induced behavioral impairments, including by blocking A2A receptors. In addition, it attenuated the oxidative stress induced by binge drinking by alternative A2A receptor pathways. Blockade of A2A receptors increased LTP levels in mPFC and vHIP, however decreased in dHIP. Conclusion: Caffeine showed neuroprotection in behavioral changes and oxidative stress induced by the binge drinking model in adolescent rats. In addition, blockade of A2A receptors mitigated the observed behavioral changes, with improvement of LTP levels in the prefrontal cortex and hippocampus, which suggests the contribution of this pathway to neuroprotection in deficits induced by ethanol exposure during adolescence.