Effect of endurance exercise training on the expression of GFAP, S100B, and NSE in the striatum of chronic/progressive mouse model of Parkinson's disease

Abstract

Goals and Objectives: Parkinson's disease (PD) is one of the most common neurodegenerative diseases in elderly. Glial fibrillary acidic protein (GFAP), calcium-binding protein (S100B), and neuron-specific enolase (NSE) are brain damage markers. The main goal of this study is to investigate the expression of these markers in the striatum (ST) of chronic/progressive mouse model of PD, and to study the effect of endurance exercise training on the expression of those markers. Materials and Methods: In this study, forty C57BL/6 albino mice were randomly divided into four groups. Sedentary control (SC, n = 10), exercise control (ExC, n = 10), sedentary Parkinson's (SPD, n = 10), and exercised Parkinson's (ExPD, n = 10). Chronic Parkinsonism was induced by injecting the animals with 10 doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (25 mg/kg) and probenecid (250 mg/kg) over 5 weeks. Modified human treadmill was used to train the mice at a speed of 18 m/min, 0 degrees of inclination, 40 min/day, 5 days/week for 4 weeks. At the end of exercise training, we examined the expression of these markers on the striatum of the four animal groups using immunohistochemistry. Results and Discussion: Parkinsonism increases the expression of NSE, S100B, and GFAP in the ST, p value P < 0.001, < 0.05, and < 0.7 respectively compared with control group. Exercise training decreases the expression of NSE, S100B, and GFAP in the exercised PD mice compared with sedentary PD mice p value < 0.005, < 0.02, and < 0.40 respectively. Conclusion: Treadmill exercise training decreased the expression of brain damage markers in the striatum of chronic Parkinsonian mice, which can partially explain the beneficial neuroprotective role of exercise in patients with PD.

The effects of aerobic exercise training on oxidant–antioxidant balance, neurotrophic factor levels, and blood–brain barrier function in obese and non-obese men

“… 52 reported a negative correlation between serum S100β levels and total antioxidant status ( r = −0.64). Moreover, Al-Jarrah and Jamous 53 previously reported that treadmill exercise training decreased S100β and NSE expression in a Parkinson's disease mouse model, supporting the results of this study. In addition, even though serum S100β and NSE levels are blood biomarkers for BBB disruption and a BBB permeability increase, 21 , 54 future studies analyzing circulating tight junction proteins and matrix metalloproteinases may more specifically reflect BBB function because S100β is expressed in various peripheral tissues, including skeletal muscle, and NSE reflects brain damage.…”

Aerobic Physical Exercise Improved the Cognitive Function of Elderly Males but Did Not Modify Their Blood Homocysteine Levels

“…Furthermore, our hypothesis is that the physical exercise increased the plasma levels of brain-derived neurotrophic factor, which plays an important role in neuroplasticity and participates in neural transmission and modulation as well as cell proliferation and neurogenesis, improving cognitive function [ 38 , 39 , 40 , 41 ]. Exercise can also decrease the expression of the enzyme neuron-specific enolase and the protein S100B that may worsen cognition [ 42 ]; the assessment of these variables could be important to explain our results and will be our focus in the future.…”

Clinical neurorestorative progress in Parkinson&#39;s disease

“…Al-Jarrah et al 81 found that endurance exercise training could promote angiogenesis in a mouse model of PD. In addition, they found this training could decrease the expression of brain damage markers in the striatum, 82 possibly by decreasing the level of neuronal nitric oxide. 83 Strong evidence showed that long-term aerobic exercise could help functional motor and limbic circuits' reorganization in a rat model of PD 84 and that longer-duration vibration training could significantly increase the number of nigrostriatal dopaminergic neurons.…”