22 October 2018 : Animal Research
Interleukin-1 Beta and Tumor Necrosis Factor Alpha Upregulation and Nuclear Factor Kappa B Activation in Skeletal Muscle from a Mouse Model of Chronic/Progressive Parkinson DiseaseNour Erekat1ABCDEFG*, Muhammed D. Al-Jarrah2BCDEF
Med Sci Monit 2018; 24: ANS7524-7531
BACKGROUND: Skeletal muscle atrophy has been reported in patients with Parkinson disease (PD). The purpose of this study was to examine the potential implication of interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNFα), and nuclear factor kappa B (NF kappa B) in skeletal muscle atrophy following PD induction.
MATERIAL AND METHODS: Chronic Parkinsonism was induced in 10 albino mice by MPTP/probenecid treatment, while 10 other albino mice remained without treatment and were subsequently used as controls. Gastrocnemius muscles were examined for the expression of IL-1β and TNF-α, as well as the nuclear localization of NF kappa B, indicative of its activation, using immunohistochemistry in the 2 different groups.
RESULTS: IL-1β and TNF-α expression and NF kappa B nuclear localization were significantly higher in the PD skeletal muscle compared with those in the controls (P value <0.01).
CONCLUSIONS: The present data are indicative of an association of PD with IL-1β and TNF-α upregulation and NF kappa B activation in gastrocnemius muscles, potentially promoting the atrophy frequently observed in PD.
Keywords: Parkinsonian Disorders
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