Combination of Aquatic Exercise with COQ10 Supplementation Improves Oxidative Stress, PTX3 and NF200 Protein Expression in Animal Model of Multiple Sclerosis

Background: Multiple sclerosis (MS) is a prevalent neurodegenerative disease characterized by axon degeneration and demyelination. Among noninvasive approaches for controlling/treating MS, physical training and antioxidant products such as coenzyme Q10 (CoQ10) are highly recommended. This study assessed the effects of aquatic exercise (EX) and CoQ10 on oxidative stress (OS) markers in an animal model of demyelination. Objectives: The present study aimed to examine the influence of CoQ10 supplementation and EX on OS indices, glial cells, pentraxin-3 (PTX3), Forkhead Box P3 (FOXP3), and neurofilament 200 (NF200) protein expression in demyelinated rats. Methods: A total of forty-nine 12 weeks old male Wistar rats with the weight of 250 ± 50 g, were randomly assigned to seven groups: Healthy control group, healthy+EX group, healthy+COQ10 group, MS group, MS+EX group, MS+COQ10 group, MS+EX+COQ10 group. The MS model induced by cuprizone (CPZ) powder that was incorporated for a duration of 6 weeks into the animals’ diet at a weight ratio of 0.5%. The exercise protocol consisted of swimming in a water pool for 30 minutes, five days a week, over the course of 6 weeks. The COQ10 supplementation was provided daily at a dosage of 150 mg/kg/day, mixed with chow for 6 weeks. The expression of PTX3 protein was assessed using the Western blot technique, while FOXP3 and NF200 protein expressions were evaluated through the ELISA method. Additionally, total antioxidant capacity (TAC), catalase (CAT), peroxidase (POX), and glutathione reductase (GR) levels were determined using the FRAP biochemical assay. Results: The findings indicated that exercise, CoQ10 supplementation, and the combination of exercise and CoQ10 significantly decreased PTX3 expression and the number of microglia, while simultaneously increasing the number of oligodendrocytes, TAC, CAT, PTX3, and GR. The combination of exercise and supplementation proved to be more effective than either intervention alone in reducing PTX3 levels or enhancing oligodendrocyte counts (P < 0.05 for all). Notably, NF200 protein expression showed no significant changes in all groups (P > 0.05). The POX levels were significantly elevated only in the EX+CoQ10 group (P < 0.05), with no significant differences in efficacy observed between exercise or CoQ10 alone for most measured indices (P > 0.05). Conclusions: The combined intervention of EX and CoQ10 supplementation demonstrates synergistic effects in mitigating OS and inflammation while promoting neuroprotection in a CPZ-induced MS model. These findings highlight the potential of integrative non-pharmacological and pharmacological approaches for managing MS. Further studies are warranted to validate these effects in human subjects.