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https://www.selleckchem.com/JAK.html These findings support that SRT1720 acts as an anti-aging agent and inhibits the inductions of inflammatory cytokines and senescence by regulating the SIRT1/acetyl-NF-κB signaling pathway and activating autophagy in senescent HDFs. Parkinson's disease (PD) is a chronic neurodegenerative disease characterized by the death of dopaminergic neurons in the substantia nigra pars compacta. Exercise training, which is incorporated both goal-based training such as task-oriented training (TOT) and aerobic training (AT), has been suggested to induce neuroprotection. However, molecular mechanisms which may underlie exercise-induced neuroprotection are still largely unknown. Thus, the aim of the present study was to investigate the effects of TOT combined with AT (TOT-AT) on serum brain-derived neurotrophic factor (BDNF), glial cell-derived growth factor (GDNF), insulin-like growth factor-1 (IGF-1), vascular endothelial growth factor (VEGF), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) levels in people with PD (PwPD). Forty PwPD were randomized into 8-week of either exercise group (n=20) or control group (n=20). The exercise group received TOT-AT while the control group received only AT. Serum BDNF, GDNF, IGF-1, VEGF, TNF-α, and IL-1β levels determined with ELISA were assessed at baseline and after training. A total of 29 PwPD completed this study. Our results showed no significant change in the serum BDNF, GDNF, IGF-1, VEGF, TNF-α, and IL-1β levels in both groups. After the intervention period, no significant difference was observed between the groups regarding the serum BDNF, GDNF, IGF-1, VEGF, TNF-α, and IL-1β levels. TOT-AT could not be an effective exercise method for changing serum concentrations of BDNF, GDNF, IGF-1, VEGF, TNF-α, and IL-1β in the rehabilitation of PD. TOT-AT could not be an effective exercise method for changing serum concentrations of BDNF, GDNF, IGF-1, VEGF, TNF-α, and IL-1β in the rehabilitation of PD

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