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Neurological Disorders

ISSN: 2329-6895

Open Access

Skilled Aerobic Exercise Reduces Endoplasmic Reticulum Stress and Dopamine Neuron Apoptosis by Activating Wnt/β-Catenin Pathway and Improves Motor Function in Pd Model Rats

Abstract

Tian Ruisi, Zhu Zhengquan, Gao Hua, Li Peishan, Yang Xinling Li and Lin Yan-xia*

Objective: To observe whether skilled aerobic exercise (SAE) could reduce endoplasmic reticulum stress (ERS) and apoptosis of dopamine neuron by activating Wnt/β-catenin pathway and improves motor function in Parkinson' s disease (PD) model rats.

Methods: The PD models were established by injection into the right SNC (substantia nigra, compact part) and VTA (ventral tegmental area) on the rat stereolocator with 6-hydroxydopamine (6-OHDA). A cylindrical test was used to was used to test motor function. The expression of tyrosine hydroxylase (TH) in midbrain was detected by immunohistochemistry, the expression of genes and proteins related to the Wnt/β-catenin pathway was detected by Western blot. The level of Irisin in serum was identified through an enzyme-linke d immunosorbent assay (ELISA).

Results: It was determined that 28 days of SAE improved motor function from Parkinson disease. In model group, the expression of TH in midbrain and FNDC5 in skeletal muscle was significantly down-regulated, the content of Irisin in serum decreased, the expression level of Bip/Grp78 and CHOP was up-regulated, the expression level of Wnt, β-catenin and P-GSK3β (Ser9) were down-regulated, while P-GSK3β (Tyr216) was up-regulated, the movement ability of forelimbs decreased (P<0.05), and the rotation behavior induced by Apo significantly increased in model group (P<0.05).

Conclusion: Mid-long term SAE could up-regulate the expression of FNDC5 in skeletal muscle, increase the content of Irisin in serum, reduce the level of ERS in midbrain, increase the activity of Wnt/β-catenin pathway, down-regulate the activity of Gsk3β, reduce the apoptosis of DA neurons in midbrain substantia nigra, and improve the motor function of PD model rats.

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