Treadmill exercise training could attenuate the upregulation of Interleukin-1 beta and tumor necrosis factor alpha in the skeletal muscle of mouse model of chronic/progressive Parkinson disease
Affiliations: [a] Department of Rehabilitation Sciences, Faculty of Applied Medical Sciences, Jordan University of Science and Technology, Irbid, Jordan
| [b] Department of Anatomy, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan
Correspondence:
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Address for correspondence: Muhammed D. Al-Jarrah, Jordan University of Science and Technology, Faculty of Applied Medical Sciences, Department of Rehabilitation Sciences, P.O. Box 3030, Irbid 22110, Jordan. E-mail: jarrahm@just.edu.jo.
Abstract: BACKGROUND:Induction of Parkinson disease (PD) causes interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) upregulation in gastrocnemius skeletal muscles. Endurance exercise suppresses iNOS and HSP90 overexpression in PD skeletal muscle. The purpose of this study is to test the impact of treadmill exercise training on PD-associated IL-1β and TNF-α upregulation in the gastrocnemius muscle. METHODS:Thirty normal albino mice were randomly selected and divided into three equal groups: sedentary control (SC), sedentary PD (SPD), and Exercised PD (EPD). Chronic Parkinsonism was induced by treating mice in the SPD and EPD groups with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and probenecid (MPTP/p). Gastrocnemius muscles were examined for the expression of IL-1β and TNF-α using immunohistochemistry in the three different groups. RESULTS:Endurance exercise training significantly decreased both IL-1β and TNF-α expression in skeletal muscle in EPD (P value < 0.01) compared with that in the SPD. CONCLUSION:Our present data suggest that PD-induced upregulation of IL-1β and TNF-α in the gastrocnemius muscle could be reversed following endurance exercise training. Accordingly, IL-1β and TNF-α might be considered therapeutically to ameliorate skeletal muscle abnormalities characterizing PD.
