Neuroprotective effects of strength training in a neuroinflammatory animal model

Abstract

Background The preventive role of muscular strength on diminishing neuroinflammation is yet unknown. In this study, the role of the prophylactic muscular strength exercise was investigated in order to verify whether it would diminish cognitive alterations and modify the antioxidant intracellular scenery in an animal neuroinflammatory model in of the CA1 region of the hippocampus. Methods The animals received muscular strength training (SE) three times a week for eight weeks. Subsequently, the stereotaxic surgery was performed with an intra-hippocampal infusion of either saline solution (SAL) or lipopolysaccharide (LPS). Next, we performed the behavioral tests: object recognition and social recognition. Then, the animals were euthanized, and their hippocampus and prefrontal cortex were collected. In another moment, we performed the dosage of the antioxidant activity and histological analysis. Results The results showed that the muscular strength exercises could show a beneficial prophylactic effect in the cognitive deficiencies caused by acute neuroinflammation. Regarding oxidative stress, there was an increase in catalase enzyme activity (CAT) in the group (SE + LPS) compared to the control groups (p < 0.05). As for the cognitive alterations, there were found in the (SE + LPS) group, diminishing the mnemonic hazard of the discriminative and social memories compared to the control groups (p < 0.05). Conclusion We concluded, therefore, that the exercise performed prophylactically presents a protective effect capable of minimizing such mnemonic deficits and increasing catalase enzyme activity in rats that suffered a local neuroinflammatory process in the hippocampus.

New perspective for an old drug: Can naloxone be considered an antioxidant agent?

“…Previous extensive literature indicates that the cells are constantly exposed to ROS whose increase above a given level results in oxidative stress [ 33 ]. Exposure to H 2 O 2 triggers a rise of ROS above basal levels that causes damage in cells [ 21 , 23 ].…”

“…As it is well known, oxidative stress is involved in the induction of apoptosis [ 35 ] and several studies have reported that the overproduction of ROS causes apoptosis [ 33 , 35 , 36 ]. Notably, NLX in our study reduced apoptotic cells at both of the concentrations examined in the presence of H 2 O 2 exposure.…”