Association of exercise-induced autophagy upregulation and apoptosis suppression with neuroprotection against pharmacologically induced Parkinson's disease

Jang, Yongchul; Hwang, Dong Joo; Koo, Jung Hoon; Um, Hyun Seob; Lee, Nam Hee; Yeom, Dong Cheol; Lee, Youngil; Cho, Joon Yong

doi:10.20463/jenb.2018.0001

Association of exercise-induced autophagy upregulation and apoptosis suppression with neuroprotection against pharmacologically induced Parkinson's disease

Jang, Y., Hwang, D. J., Koo, J. H., Um, H. S., Lee, N. H., Yeom, D. C., Lee, Y., & Cho, J. Y. (2018). Association of exercise-induced autophagy upregulation and apoptosis suppression with neuroprotection against pharmacologically induced Parkinson’s disease. Journal of Exercise Nutrition & Biochemistry, 22(1), 1-8. doi:10.20463/jenb.2018.0001

Details

Type: Academic Journal Article
Title: Association of exercise-induced autophagy upregulation and apoptosis suppression with neuroprotection against pharmacologically induced Parkinson's disease
Contributor(s): Jang, Yongchul (author)
Hwang, Dong Joo (author)
Koo, Jung Hoon (author)
Um, Hyun Seob (author)
Lee, Nam Hee (author)
Yeom, Dong Cheol (author)
Lee, Youngil (author)
Cho, Joon Yong (author)
Located In: Journal of Exercise Nutrition & Biochemistry
ISSN: 2233-6834
Volume: 22
Issue: 1
Start Page: 1
End Page: 8
Date: 2018
DOI: 10.20463/jenb.2018.0001
Use/Reproduction: 2018 Yongchul Jang et al; License Journal of Exercise Nutrition and Biochemistry. This is an open access article distributed under the terms of the creative commons attribution license (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract: [Purpose] We investigated whether treadmill exercise (TE)-induced neuroprotection was associated with enhanced autophagy and reduced apoptosis in a mouse model of pharmacologically induced Parkinson's disease (PD). [Methods] PD was induced via the administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). C57BL/6 male mice were randomly assigned to the following three groups: control (C57BL, n=10), MPTP with probenecid (MPTP/C, n=10), and MPTP/C plus exercise (MPTP-TE, n=10). The MPTP-TE mice performed TE training (10 m/min, 60 min/day, 5 days/week) for 8 weeks. The rotarod test was used to assess motor function. [Results] TE restored MPTP/P-induced motor dysfunctionand increased tyrosine hydroxylase levels. Furthermore, TE diminished the levels of α-synuclein (α-syn), a neurotoxin; modulated the levels of autophagy-associated proteins, including microtubule-associated protein 1 light chain 3-II, p62, BECLIN1, BNIP3, and lysosomal-associated membrane protein-2, which enhanced autophagy; inhibited the activation of proapoptotic proteins (caspase-3 and BAX);and upregulated BCL-2, an antiapoptosis protein. [Conclusion] Taken together, these results suggested that the TE-induced neuroprotection against MPTP-induced cell death was associated with enhanced autophagy and neuronal regeneration based on the findings of inhibited proapoptotic events in the brains of the TE-trained animals.
Subject(s): treadmill exercise
Parkinson’s disease
α-synuclein
autophagy
apoptosis
PID: uwf:23860