신경세포로 분화된 PC12 세포의 과산화수소에 의한 손상에 대한 15-deoxy-D12,14-Prostagladin J2 (15d-PGJ2)의 세포보호효과Cytoprotective Effect of 15-deoxy-Delta(12,14) Prostaglandin J2 (15d-PGJ2) against H2O2 Induced Death of Neuronally-differentiated PC12 Cells
- Other Titles
- Cytoprotective Effect of 15-deoxy-Delta(12,14) Prostaglandin J2 (15d-PGJ2) against H2O2 Induced Death of Neuronally-differentiated PC12 Cells
- Authors
- 오동호; 고성호; 정부; 박기형; 김현영; 송치원; 김영철; 김주한; 김명호; 김승현
- Issue Date
- Feb-2006
- Publisher
- 대한신경과학회
- Keywords
- Apoptosis; Neurodegenerative disease; Antioxidants; Cytochrome c; Caspase-3
- Citation
- 대한신경과학회지, v.24, no.1, pp.58 - 65
- Indexed
- KCI
- Journal Title
- 대한신경과학회지
- Volume
- 24
- Number
- 1
- Start Page
- 58
- End Page
- 65
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/181750
- ISSN
- 1225-7044
- Abstract
- Background: Neurodegenerative diseases are associated with oxidative stress. Antioxidants including 15-deoxy- Delta (12,14) prostaglandin J2 (15d-PGJ2) have been tried as potential therapeutic regimens of the experimental model of neurodegenerative disease. In this study, we investigated the neuroprotective role of 15d-PGJ2 on cytochrome c mediated apoptotic signals in oxidative stress injured neuronally-differentiated PC12 cells (nPC12 cells) by exposing them to H2O2. Methods: Following 100 µM H2O2 exposure, the viability of nPC12 cells (pretreated with 15d-PGJ2 vs. not pretreated) was evaluated by using MTT assay. Immunoreactivity (IR) of cytochrome c, caspase-3, and poly (ADP-ribose) polymerase (PARP) was examined by using a Western blot. Results: In this study, 15d-PGJ2 pretreated nPC12 cells showed an increase in cell viability until the concentrations of 15d-PGJ2 reached up to 4 µM, but there was no increment of cell viability in higher concentrations. The inhibition of cytochrome c release, activation of caspase-3, and cleavage of PARP were demonstrated by the pretreatment of 15d-PGJ2 up to 4 µM. However, these were not observed in the pretreatment with 8 µM 15d-PGJ2. Conclusions: These data show that 15d-PGJ2 affects the apoptotic pathway through downstream signals including cytochrome c and caspase-3 pathway. Therefore, these results suggest that 15d-PGJ2 could be a new potential therapeutic candidate for the oxidative stress-injury model of neurodegenerative diseases.
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