Jorjani Biomedicine Journal

Background and Objective: Trimethyltin (TMT) is an organotin neurotoxin which causes cognitive disorders by the induction of selective damage in hippocampus. The present study evaluates the effect of 8-week swimming exercise (EX) and Gallic acid (GA) for working and avoidance memory, hippocampal oxidative stress indices and brain neurotrophic factor expression (BDNF) in rats after TMT intoxication.
Material and Methods: In this experimental study, 40 Wistar mature male rats were randomly put in 5 groups of control, TMT+NS, TMT+GA200, TMT+EX, TMT+GA200+EX. 24 hours after TMT intoxication (8mg/kg), 8 weeks of swimming exercise (3 sessions per week), and treatment with GA (200mg/kg) were done. Then, the evaluation of working and passive avoidance memory was performed respectively by the use of Y maze and shuttle box. Hippocampal level of catalase (CAT), total antioxidant capacity (TAC) and BDNF were done by ELISA method, and content of malondialdehyde (MDA) was performed by thiobarbituric acid (MDA). Statistical differences between groups were analyzed by two-way ANOVA and Bonferroni post hoc test.
Results: The significant decrease in the percentage of alteration behaviors, latency time to the dark room, along with BDNF, CAT, TAC and increase of MDA were seen in TMT+NS group compared to control group (p<0.01). Swimming exercise in the interaction with GA ameliorates working and avoidance memory by increasing BDNF, CAT, TAC, and decrease of MDA compared to TMT+NS group (p<0.05).
Conclusion: It seems that swimming exercise and GA administration improves cognitive symptoms following TMT intoxication simultaneously by decreasing oxidative stress and increasing BDNF expression.

Background: Performing exercise training with various protocols, especially aquatic exercises, can be effective against the harmful effects of Multiple Sclerosis. Therefore, the present study aimed to investigate the effect of six weeks of swimming training on the Caspase-1, TGF-β1, and IFN-γ protein content in the hippocampal tissue of rats with Multiple Sclerosis.
Methods: Twenty-one Wistar rats were divided into three equal groups: (1) Healthy control, (2) Multiple Sclerosis control, and (3) Multiple Sclerosis swimming. After two weeks of adaptation to the laboratory environment, the Multiple Sclerosis groups were induced by adding cuprizone to their diet. Six weeks of swimming training were then performed. Forty-eight hours after the last session, hippocampal tissue was isolated to examine Caspase-1, TGF-β1, and IFN-γ protein content. To analyze the data, one-way analysis of variance was used with a significance level of 0.05.
Results: Findings showed that the induction of Multiple Sclerosis in rats caused a significant increase in TGF-β1 and Caspase-1 protein content (P-Value=0.001) and a significant decrease in IFN-γ (P-Value =0.001). After six weeks of swimming, there was a significant decrease in Caspase-1 (P-Value =0.001) and a significant increase in IFN-γ (P-Value =0.001) protein content; however, there was no significant decrease in TGF-β1 protein content (P-Value =0.1).
Conclusion: Based on the findings of this study, it can be concluded that swimming, as a non-pharmacological intervention, has a protective effect on nerves by reducing factors related to inflammation and cell death, which may have beneficial effects on memory information processing in Multiple Sclerosis disease.