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
Autor: | Nour S. Erekat, Muhammed Al-Jarrah |
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Rok vydání: | 2019 |
Předmět: |
030506 rehabilitation
medicine.medical_specialty Interleukin-1beta Physical Therapy Sports Therapy and Rehabilitation Mice 03 medical and health sciences chemistry.chemical_compound Gastrocnemius muscle 0302 clinical medicine Downregulation and upregulation Endurance training Physical Conditioning Animal Internal medicine medicine Animals Muscle Skeletal Tumor Necrosis Factor-alpha business.industry MPTP Parkinsonism Rehabilitation MPTP Poisoning Skeletal muscle medicine.disease Up-Regulation Probenecid Endocrinology medicine.anatomical_structure chemistry Tumor necrosis factor alpha Neurology (clinical) 0305 other medical science business 030217 neurology & neurosurgery medicine.drug |
Zdroj: | NeuroRehabilitation. 43:501-507 |
ISSN: | 1878-6448 1053-8135 |
Popis: | 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 |
Databáze: | OpenAIRE |
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