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Neuroprotective effects of endurance exercise against neuroinflammation in MPTP-induced Parkinson's disease mice.
Jang, Yongchul; Koo, Jung-Hoon; Kwon, Insu; Kang, Eun-Bum; Um, Hyun-Seob; Soya, Hideaki; Lee, Youngil; Cho, Joon-Yong.
Afiliación
  • Jang Y; Exercise Biochemistry Laboratory, Korea National Sport University, 88-15 Oryun-dong, Songpa-gu, Seoul 138-763, Republic of Korea; Exercise Biochemistry Laboratory, University of West Florida, 11000 University Pkwy, Bldg. 72, Pensacola, FL 32514, USA.
  • Koo JH; Exercise Biochemistry Laboratory, Korea National Sport University, 88-15 Oryun-dong, Songpa-gu, Seoul 138-763, Republic of Korea.
  • Kwon I; Exercise Biochemistry Laboratory, University of West Florida, 11000 University Pkwy, Bldg. 72, Pensacola, FL 32514, USA.
  • Kang EB; Exercise Biochemistry Laboratory, Korea National Sport University, 88-15 Oryun-dong, Songpa-gu, Seoul 138-763, Republic of Korea.
  • Um HS; Department of Exercise Prescription, Kon-Yang University, 119 Daehangro, Nonsan city, Chungnam 320-711, Republic of Korea.
  • Soya H; Laboratory of Exercise Biochemistry and Neuroendocrinology, Faculty of Health and Sports Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8574, Japan.
  • Lee Y; Exercise Biochemistry Laboratory, University of West Florida, 11000 University Pkwy, Bldg. 72, Pensacola, FL 32514, USA.
  • Cho JY; Exercise Biochemistry Laboratory, Korea National Sport University, 88-15 Oryun-dong, Songpa-gu, Seoul 138-763, Republic of Korea. Electronic address: chojy86@knsu.ac.kr.
Brain Res ; 1655: 186-193, 2017 01 15.
Article en En | MEDLINE | ID: mdl-27816415
Parkinson's disease (PD) is one of the main degenerative neurological disorders accompanying death of dopaminergic neurons prevalent in aged population. Endurance exercise (EE) has been suggested to confer neurogenesis and mitigate the degree of seriousness of PD. However, underlying molecular mechanisms responsible for exercise-mediated neuroprotection against PD remain largely unknown. Given the relevant interplay between elevated α-synuclein and neuroinflammation in a poor prognosis and vicious progression of PD and anti-inflammatory effects of EE, we hypothesized that EE would reverse motor dysfunction and cell death caused by PD. To this end, we chose a pharmacological model of PD (e.g., chronic injection of neurotoxin MPTP). Young adult male mice (7 weeks old) were randomly divided into three groups: sedentary control (C, n=10), MPTP (M, n=10), and MPTP + endurance exercise (ME, n=10). Our data showed that EE restored motor function impaired by MPTP in parallel with reduced cell death. Strikingly, EE exhibited a significant reduction in α-synuclein protein along with diminished pro-inflammatory cytokines (i.e., TNF-α and IL-1ß). Supporting this, EE prevented activation of Toll like receptor 2 (TLR2) downstream signaling cascades such as MyD88, TRAF6 and TAK-1 incurred by in MPTP administration in the striatum. Moreover, EE reestablished tyrosine hydroxylase at levels similar to C group. Taken together, our data suggest that an EE-mediated neuroprotective mechanism against PD underlies anti-neuroinflammation conferred by reduced levels of α-synuclein. Our data provides an important insight into developing a non-pharmacological countermeasure against neuronal degeneration caused by PD.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Cuerpo Estriado / Intoxicación por MPTP / Terapia por Ejercicio / Porción Compacta de la Sustancia Negra / Neuroprotección Límite: Animals Idioma: En Revista: Brain Res Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Cuerpo Estriado / Intoxicación por MPTP / Terapia por Ejercicio / Porción Compacta de la Sustancia Negra / Neuroprotección Límite: Animals Idioma: En Revista: Brain Res Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos