Abstract
The heavy and episodic EtOH drinking pattern, equivalent to weekend consumption, characterizes the binge-drinking pattern and promotes a misbalance of encephalic metabolic functions, concurring to neurodegeneration and cerebral dysfunction. And for being a legal drug, it has global public health and social relevance. In this way, we aimed to investigate the effects of physical training, in a treadmill, on the deleterious effects of EtOH on hippocampal functions, related to memory and learning. For this, we used 40 Wistar rats, divided into four groups: Control group, Trained group (trained animals with doses of distilled water), EtOH group (nontrained animals with doses of 3 g/kg/day of EtOH, 20% w/v), and Trained+EtOH group (trained animals exposed to EtOH). The physical exercise was performed by running on a treadmill for 5 days a week for 4 weeks, and all doses of EtOH were administered through intragastric gavage in four repeated cycles of EtOH in binge. After the experimental period, the animals were submitted to the object recognition task and Morris water maze test, and after being euthanized, the blood and hippocampus were collected for Trolox Equivalent Antioxidant Capacity (TEAC), Reduced Glutathione Content (GSH), and Nitrite and Lipid Peroxidation (LPO) level measurements. Our results showed that EtOH caused marked oxidative stress and mnemonic damage, and the physical exercise promoted neuroprotective effects, among them, the modulation of oxidative biochemistry in plasma (by restoring GSH levels) and in the hippocampus (by reducing LPO levels and increasing antioxidant parameters) and cognitive function improvement. Therefore, physical exercise can be an important prophylactic and therapeutic tool in order to ameliorate and even prevent the deleterious effects of EtOH on cognitive functions.
Highlights
Ethanol (EtOH) is a psychotropic drug that generates behavioral changes and may lead to addiction, i.e., dependency
This is quite evident in the hippocampus, where the consumption of EtOH in the intermittent model promotes the reduction of neurogenesis, hippocampal volume, synaptic communication, and neurotrophins associated with neuroplasticity as a brain-derived neurotrophic factor (BDNF) [2, 5,6,7,8], which is strongly associated with cognitive impairments
This nonpharmacological therapeutic tool is associated with Trolox Equivalent Antioxidant Capacity (TEAC) and GSH level restoration in the hippocampus of rats exposed to EtOH and the reduction of Lipid Peroxidation (LPO) levels into the basal state, comparable to nonexposed animals
Summary
Ethanol (EtOH) is a psychotropic drug that generates behavioral changes and may lead to addiction, i.e., dependency. EtOH has been associated with short- and long-term neuropsychological effects, and the increased prevalence of the binge-drinking pattern during adolescence, Oxidative Medicine and Cellular Longevity when the brain is still in development and maturation, constitutes an important global health problem since it predisposes individuals to dependence and comorbidities [2,3,4] This is quite evident in the hippocampus, where the consumption of EtOH in the intermittent model promotes the reduction of neurogenesis, hippocampal volume, synaptic communication, and neurotrophins associated with neuroplasticity as a brain-derived neurotrophic factor (BDNF) [2, 5,6,7,8], which is strongly associated with cognitive impairments. The beneficial effects of the association between physical exercise and EtOH consumption are not completely understood, still requiring elucidation of the main mechanism by which physical training may help alcoholic drinkers, especially over cognitive functions associated with hippocampal formation
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