KMID : 0624620150480070395
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BMB Reports 2015 Volume.48 No. 7 p.395 ~ p.400
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Protective effects of PEP-1-Catalase on stress-induced cellular toxicity and MPTP-induced Parkinson¡¯s disease
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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
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Abstract
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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.
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KEYWORD
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Parkinson¡¯s disease, ROS, PEP-1-Catalase, Protein therapy, Dopaminergic neuron
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