the interactive effects of the aerobic exercise and vitamin e supplementation on parkinson’s rat model

Objective: in parkinson’s disease (pd), mitochondrial defects and oxidative stress cause an increase in free radicalsand the death of dopaminergic neurons in the substantia nigra. by preventing lipid peroxidation and protecting againstperoxide 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 theresult of changes in the mitochondrial mitophagy and dynamics system. this study aimed to investigate the interactiveeffects 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 tissueof 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 wascarried out for six weeks and 5 sessions per week and each session lasted 15-22 minutes. ve was also taken orallyat 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 nosignificant 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.