트레드밀 운동이 파킨슨 유도 모델 쥐의 α-synuclein 발현과 미토콘드리아 구조적 역동성에 미치는 영향
The Effect of Treadmill Exercise on α-synuclein and Mitochondrial Dynamic in The Mouse Model of Parkinson’s Disease
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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 (12 m/min, 60 min/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.
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 (12 m/min, 60 min/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.
참고문헌 (44)
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