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The effect of treadmill exercise on α-synuclein and mitochondrial dynamic in the MPTP-induced mice model of Parkinson’s Disease
Jung Hoon Koo
korea national sport university, seoul, Korea
Correspondence  Jung Hoon Koo , Tel: 010-2275-6129, Fax: 02-410-6945, Email: mt634@knsu.ac.kr
Received: July 26, 2016;  Accepted: October 15, 2016.  Published online: October 15, 2016.
ABSTRACT
PURPOSE:
The purpose of this study was to investigate the effects of treadmill exercise on motor function, α-synuclein(α-syn), neuronal cell survival, mitochondrial dynamic-related proteins, and sirtuin-3(SIRT-3) in the MPTP-induced mice model of Parkinson’s disease (PD).
METHODS:
Twenty four mice model of PD were divided into three groups: (1) Sham control (Sham, n=8), (2) MPTP treatment (MPTP, n=8) and (3) MPTP-Exercise (MPTP-E, n=8). MPTP-E mice group were performed to exercise on a treadmill for 8 weeks (12m/min, 60min/day, 5 days/week). In addition, we conducted Rota-rod test to evaluate the motor function. And then, substantia nigra (SN) was evaluated to determine whether any changes in the α-syn, neuronal cell survival, SIRT-3, mitochondrial fission, and fusion proteins.
RESULTS:
Treadmill exercise rescued motor deficits by reducing α-syn expression and alleviating neuronal cell death in the MPTP-induce mice model of PD. In addition, treadmill exercise increased mitochondrial fusion-related protein(Opa1, Mfn1, Mfn2) and decreased mitochondrial fission-related protein(Fis1, Drp1) possibly via activating SIRT-3 expression in the MPTP-induce mice model of PD.
CONCLUSIONS:
Treadmill exercise improved motor function by inhibiting neurotoxicity and improving mitochondrial dynamic via reducing α-syn expression and activating SIRT-3 expression. These results indicating that improving mitochondrial dysfunction via treadmill exercise may be potent strategy to alleviate the PD pathogenesis.
Key words: Parkinson’s disease; α-synuclein; treadmill exercise; mitochondrial dysfunction; mitochondrial dynamic; sirtuin-3
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