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KMID : 0624620150480070395
BMB Reports
2015 Volume.48 No. 7 p.395 ~ p.400
Protective effects of PEP-1-Catalase on stress-induced cellular toxicity and MPTP-induced Parkinson¡¯s disease
Eom Seon-Ae

Kim Dae-Won
Shin Min-Jea
Ahn Eun-Hee
Chung Seok-Young
Sohn Eun-Jeong
Jo Hyo-Sang
Jeon Su-Jeong
Kim Duk-Soo
Kwon Hyeok-Yil
Cho Sung-Woo
Han Kyu-Hyung
Park Jin-Seu
Eum Won-Sik
Choi Soo-Young
Abstract
Parkinson¡¯s disease (PD) is a neurodegenerative disability caused by a decrease of dopaminergic neurons in the substantia nigra (SN). Although the etiology of PD is not clear, oxidative stress is believed to lead to PD. Catalase is antioxidant enzyme which plays an active role in cells as a reactive oxygen species (ROS) scavenger. Thus, we investigated whether PEP-1-Catalase protects against 1-methyl-4-phenylpyridinium (MPP+) induced SH-SY5Y neuronal cell death and in a 1-methyl- 4-phenyl-1,2,3,6-trtrahydropyridine (MPTP) induced PD animal model. PEP-1-Catalase transduced into SH-SY5Y cells significantly protecting them against MPP+-induced death by decreasing ROS and regulating cellular survival signals including Akt, Bax, Bcl-2, and p38. Immunohistochemical analysis showed that transduced PEP-1-Catalase markedly protected against neuronal cell death in the SN in the PD animal model. Our results indicate that PEP-1-Catalase may have potential as a therapeutic agent for PD and other oxidative stress related diseases.
KEYWORD
Parkinson¡¯s disease, ROS, PEP-1-Catalase, Protein therapy, Dopaminergic neuron
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