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 Disease.

Abstract

BackgroundSkeletal 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 (TNF-α), and nuclear factor kappa B (NF kappa B) in skeletal muscle atrophy following PD induction.Material/MethodsChronic 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.ResultsIL-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).ConclusionsThe 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.