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Phosphodiesterase Ⅲ Inhibitor Cilostazol Protects Amyloid β-Induced Neuronal Cell Injury via Peroxisome Proliferator-Activated Receptor-γ Activation
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논문 기본 정보

Type
Academic journal
Author
Sun Haeng Park (부산대학교) Ji Hyun Kim (부산대학교) Sun Sik Bae (부산대학교) Ki Whan Hong (부산대학교) Byung Tae Choi (부산대학교) Hwa Kyoung Shin (부산대학교)
Journal
Korean Society Of Life Science Journal of Life Science Vol.21 No.5 KCI Accredited Journals
Published
2011.5
Pages
647 - 655 (9page)

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Phosphodiesterase Ⅲ Inhibitor Cilostazol Protects Amyloid β-Induced Neuronal Cell Injury via Peroxisome Proliferator-Activated Receptor-γ Activation
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The neurotoxicity of aggregated amyloid β (Aβ) has been implicated as a critical cause in the pathogenesis of Alzheimer’s disease (AD). It can cause neurotoxicity in AD by evoking a cascade of apoptosis to neuron. Here, we investigated the neuroprotective effects of cilostazol, which acts as a phosphodiesterase Ⅲ inhibitor, on Aβ<SUB>25-35</SUB>-induced cytotoxicity in mouse neuronal cells and cognitive decline in the C57BL/6J AD mouse model via peroxisome proliferator-activated receptor (PPAR)-γ activation. Aβ<SUB>25-35</SUB> significantly reduced cell viability and increased the number of apoptotic-like cells. Cilostazol treatment recovered cells from Aβ-induced cell death as well as rosiglitazone, a PPAR-γ activator. These effects were suppressed by GW9662, an antagonist of PPAR-γ activity, indicative of a PPAR-γ -mediated signaling. In addition, cilostazol and rosiglitazone also restored PPAR-γ activity levels that had been altered as a result of Aβ<SUB>25-35</SUB> treatment, which were antagonized by GW9662. Furthermore, cilostazol also markedly decreased the number of apoptotic-like cells and decreased the Bax/Bcl-2 ratio. Intracerebroventricular injection of Aβ<SUB>25-35</SUB> in C57BL/6J mice resulted in impaired cognitive function. Oral administration of cilostazol (20 ㎎/㎏) for 2 weeks before Aβ25-35 injection and once a day for 4 weeks post-surgery almost completely prevented the Aβ<SUB>25-35</SUB>-induced cognitive deficits, as did rosiglitazone. Taken together, our findings suggest that cilostazol could attenuate Aβ<SUB>25-35</SUB>-induced neuronal cell injury and apoptosis as well as promote the survival of neuronal cells, subsequently improving cognitive decline in AD, partly because of PPAR-γ activation. The phosphodiesterase Ⅲ inhibitor cilostazol may be the basis of a novel strategy for the therapy of AD.

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Materials and Methods
Results
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UCI(KEPA) : I410-ECN-0101-2013-470-000633704