RESUMO
OBJECTIVE: In Parkinson's disease (PD), mitochondrial defects and oxidative stress cause an increase in free radicals and the death of dopaminergic neurons in the substantia nigra. By preventing lipid peroxidation and protecting against peroxide radicals, vitamin E is the most important antioxidant of biological membranes that can neutralize free radicals. Also, the improvement of the functional status of mitochondria can be influenced by exercise, which can be partially the result of changes in the mitochondrial mitophagy and dynamics system. This study aimed to investigate the interactive effects of six weeks of vitamin E (VE) consumption and training on the mitochondrial function [Cytochrome C (Cyt-C), Adenosine triphosphate (Atp) synthase, optical atrophy1 mitochondrial dynamics like guanosine triphosphatase (GTPase), 8-Oxodequanosin and Pten induced kinase 1 (Pink1) is a protein coding gene] in the hippocampus tissue of PD rats. MATERIALS AND METHODS: In this experimental study, 4-6-month-old Sprague-Dawley rats (mean weight 250 ± 30 g) were given parkinsonism with reserpine (2 mg/kg) and were categorized into different groups, including healthy (H), PD, VE solvent+PD (Sham), aerobic exercise+PD (AE+PD), VE+PD, AE+VE+PD. The aerobic training program was carried out for six weeks and 5 sessions per week and each session lasted 15-22 minutes. VE was also taken orally at 30 mg/kg daily. RESULTS: A six-week regimen of VE supplement along with the AE significantly reduced the Cyt-C gene expression level, also we observed a significant increase in gene expression level of the Pink1, Atp synthase and Opa1 (P<0.05). There is no significant difference was found in the level of 8-Oxog detected in hippocampal tissue samples (P>0.05). CONCLUSION: The consumption of VE along with AE may provide therapeutic effects on mitochondrial damage in PD rats.
RESUMO
Mitochondrial dysfunction is a significant feature of type 2 diabetes. MOTS-C, a peptide derived from mitochondria, has positive effects on metabolism and exercise capacity. This study explored the impact of high and moderate-intensity interval exercises on mitochondrial MOTS-C alterations and their correlation with metabolic markers in male diabetic sand rats. Thirty male sand rats were divided into six groups: control, MIIT, DM + HIIT, DM + MIIT, DM, and HIIT (5 rats each). Diabetes was induced using a high-fat diet (HFD) combined with streptozotocin (STZ). The Wistar sand rats in exercise groups underwent 8 weeks of interval training of varying intensities. Post sample collection, protein expressions of PCG-1a, AMPK, and GLUT4 were assessed through Western blot analysis, while MOTS-C protein expression was determined using ELISA. Both exercise intensity and diabetes significantly affected the levels of PCG-1a, MOTS-C, GLUT4 proteins, and insulin resistance (p < 0.001). The combined effect of diabetes status and exercise intensity on these levels was also significant (p < 0.001). However, the diabetes effect varied when comparing high-intensity to moderate-intensity exercise. The moderate-intensity exercise group with diabetes showed higher levels of PCG-1a, MOTS-C, and GLUT4 proteins and reduced insulin resistance levels (p < 0.001). Exercise intensity (p = 0.022) and diabetes (p = 0.008) significantly influenced AMPK protein levels. The interplay between diabetes status and exercise intensity on AMPK protein levels was noteworthy, with the moderate-intensity diabetes group exhibiting higher AMPK levels than the high-intensity diabetes group (p < 0.001). In conclusion, exercise elevates the levels of PCG-1a, MOTS-C, GLUT4, and AMPK proteins, regulating insulin resistance in diabetic sand rats. Given the AMPK-MOTS-C mitochondrial pathway's mechanisms, interval exercises might enhance the metabolic rates and general health of diabetic rodents.